Tetrapolar electrode system for measuring physiological events by impedance.
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Electric Conductivity↗
Biomedical subjects
W A Tacker
Publications and source records attributed to W A Tacker.
Output power and metabolic input power of skeletal muscle contracting linearly to compress a pouch in a mock circulatory system.
Output power and metabolic input power values were determined for unconditioned canine latissimus dorsi (two), gastrocnemius (seven), and triceps (three) muscles contracting linearly to cause compression of a doubly valved pouch in a hydraulic model of the circulation. The motor nerves to the muscles were stimulated tetanically with 450 msec trains of 0.1 msec pulses having a frequency of 50/sec. The muscles were contracted 10, 20, 30, and 40 times per minute and pouch output in milliliters per minute was measured directly for each muscle at each contraction (train) rate. The output power in milliwatts was determined by two methods: (1) by using the pouch output and the pressure rise imparted to the stroke volume (average power) and (2) by using the pressure-volume loop. Metabolic input power in milliwatts was determined from the oxygen consumption in milliliters per minute of the working muscle. It was found that as the pouch output was increased, the pouch output power and the metabolic input power both increased. The average power output was slightly less than that computed from the pressure-volume loop. The mean output power values, when pumping at L liters per minute, were 0.62 L (average) and 0.75 L mW/gm (pressure-volume loop) for the latissimus dorsi muscles; 0.83 L (average) and 1.16 L mW/gm (pressure-volume loop) for the gastrocnemius muscles; and 0.55 L (average) and 0.66 L mW/gm (pressure-volume loop) for the triceps muscles. The percent efficiency of energy conversion ranged from 9.2% to 17.8% for the latissimus dorsi muscles, from 5.1% to 19.5% for the gastrocnemius muscles, and from 10.5% to 27.3% for the triceps muscles. However, it should not be concluded that one muscle type is better than another on the basis of percent efficiency because efficiency does not take endurance into account. An important observation in this study relates to the large output obtained with the three linearly contracting muscle types. All were capable of pumping in excess of 1.5 L/min. A second observation relates to the absence of fatigue, although determination of endurance was not an objective in these studies.
Animals↗
Correlation of motor-evoked potential response to ischemic spinal cord damage.
The prevalence of morbidity is a major deterrent to the success of aortic aneurysm replacement operations. We have developed a model of spinal cord ischemia, based on the amplitude reduction of the motor-evoked potential, which produces approximately a 90% prevalence of paraplegia. Regional blood flow was studied with the use of radioactive microspheres, and results showed that there was a significant decrease in flow to the lumbar cord (85% reduction) during aortic occlusion, followed by a twofold to threefold hyperemia that persisted for 24 hours. Histopathologic examination of the cord revealed that the greater portion of microgliosis, spongiosis, and neuronal damage was confined to the gray matter of the cord, and its severity increased as one progressed caudally. The somatosensory-evoked potential disappeared before the motor-evoked potential L-2 signal in all dogs, with a mean disappearance time of 10.9 +/- 5.6 minutes, compared with 21 +/- 6.6 minutes for the motor-evoked potential. Both the sensory-evoked potential and the motor-evoked potential cord signal were present 24 hours later in all dogs tested. The peripheral nerve motor-evoked potential disappeared within 1 minute of cord ischemia, was not present 24 hours later, and hence appears to be too sensitive to use as an indicator of spinal cord damage. Plotting spinal cord motor-evoked potential amplitude reduction versus both histopathologic damage and regional blood flow revealed a positive correlation between motor-evoked potential amplitude reduction, decreased cord perfusion, and increased histopathologic damage. In addition, it may be possible to make inferences about the neurologic status of a subject based on the magnitude and time-course of the motor-evoked potential's amplitude reduction and wave morphology.
Animals↗
Limitations of open-chest cardiac massage after prolonged, untreated cardiac arrest in dogs.
STUDY OBJECTIVES: Open-chest cardiac massage is an effective method of resuscitation if instituted within 15 minutes of normothermic cardiac arrest that has failed to respond to ongoing closed-chest CPR efforts. The usefulness of invasive forms of CPR after various periods of untreated cardiac arrest is less certain. This study was performed to determine the effectiveness of open-chest resuscitation after prolonged periods of untreated cardiac arrest. SETTING AND DESIGN: Prospective, controlled laboratory investigation using an animal model of cardiac arrest. Open-chest cardiac massage initially was compared to standard closed-chest compression CPR. The efficacy of open-chest CPR then was evaluated after ten and 40 minutes of untreated ventricular fibrillation. TYPE OF PARTICIPANTS: Twenty mongrel dogs (24 +/- 1 kg). MEASUREMENTS AND MAIN RESULTS: After 20 minutes of untreated ventricular fibrillation, open-chest resuscitation was significantly better than closed-chest efforts for the production of coronary perfusion pressure (58 +/- 14 vs 2 +/- 1 mm Hg; P less than .05) and initial resuscitation success (five of five vs one of five; P less than .03). Open-chest cardiac massage was equally effective for initial resuscitation if begun after ten or 20 minutes of untreated ventricular fibrillation (five of five vs five of five), but if untreated ventricular fibrillation continued for 40 minutes prior to instituting open-chest massage, no resuscitation benefit was found (none of five; P less than .005). There were marked differences in 24-hour survival depending on the length of time untreated cardiac arrest continued prior to instituting open-chest resuscitation efforts. After 20 minutes of ventricular fibrillation, initial resuscitation was successful with open-chest massage, but long-term survival was poor. CONCLUSION: Open-chest cardiac massage did not produce long-term survival if untreated cardiac arrest persisted for 20 or more minutes prior to invasive resuscitation efforts.
Animals↗
Pyramidal versus extrapyramidal origins of the motor evoked potential.
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Animals↗
Comparison of canine skeletal muscle power from twitches and tetanic contractions in untrained muscle: a preliminary report.
Power output and blood flow were determined in dogs for four muscles (gastrocnemius, latissimus dorsi, rectus abdominis, and triceps) to determine effects of choice of muscle, tetany or twitch rates, force loading of the muscle, and blood flow on muscle power output. Total power for a 20-Kg dog was greatest for triceps at 0.77 watts (W) and least for rectus at 0.22 W; power per gram was greatest for gastrocnemius at 5.77 mW/g. Muscle perfusion of latissimus and rectus is greatly decreased by overstretching of the muscle. Overstretching also produces severe, persistent, power loss in latissimus and rectus muscles. Gastrocnemius and triceps tolerate stretching much better. We conclude that power can be improved without causing muscle fatigue by choice of muscle, choice of electrical stimulation parameters, linear geometry for contraction of the muscle, and matching the force load to each individual muscle.
Abdominal Muscles↗
Suprathreshold brain stimulation activates non-corticospinal motor evoked potentials in cats.
In the feline model of the motor evoked potential (MEP) test, a multiphasic spinal cord signal can be elicited in response to bipolar or transcranial brain stimulation. Previous studies have shown that signals produced by threshold stimulation travel mostly in the corticospinal tract. However, from this study we show that suprathreshold stimulation produces very large amplitude MEPs which travel in the ventral funiculus and therefore are most likely associated with extrapyramidal tract activation. The data supporting this conclusion are: (1) apparent conduction velocities of the first two large amplitude peaks are at least 80 m/s with transcranial stimulation; (2) latency of the transcranial MEP at L2 in the cord is less than or equal to 3.50 ms; (3) large amplitude, positive monophasic potentials are recorded in the ventral but not dorsal-lateral funiculus for either bipolar or transcranial MEPs; (4) both bipolar and transcranial MEPs are significantly reduced or abolished by selective lesion of the ventral funiculus. The two tracts which we believe are responsible for mediating the suprathreshold MEP in the cat are the reticulospinal and vestibulospinal tracts. This is significant because suprathreshold MEPs can be used to monitor feline ventral cord function. Furthermore, combining the use of threshold and suprathreshold MEPs may provide a differential diagnostic test for pyramidal vs. extrapyramidal motor function.
Animals↗
Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.
We studied left ventricular endomyocardial adenosine triphosphate levels in 13 large mongrel dogs before and during ventricular fibrillation induced cardiac arrest to assess whether myocardial adenosine triphosphate content could predict successful cardiopulmonary resuscitation. Endomyocardial biopsies were performed during sinus rhythm (control), after 15 min of ventricular fibrillation or 10 min of ventricular fibrillation and 5 min of open chest cardiopulmonary resuscitation, after 20 min of ventricular fibrillation and 10 min of open chest cardiopulmonary resuscitation and after 40 min ventricular fibrillation and 15-20 min open chest cardiopulmonary resuscitation. Myocardial adenosine triphosphate was measured utilizing a bioluminescence method adapted for use with endomyocardial biopsies and normalized to protein content. Left ventricular endomyocardial adenosine triphosphate content fell significantly over time from a control level of 8.88 +/- 0.9 micrograms/mg protein to 5.73 +/- 0.5 micrograms/mg protein at 15 min of cardiac arrest, to 3.4 +/- 0.4 micrograms/mg protein after 30 min of cardiac arrest and to 1.98 +/- 0.3 micrograms/mg protein after 60 min of cardiac arrest (P less than 0.001). Adenosine triphosphate levels were significantly different between animals that received 10 min of ventricular fibrillation and successful open chest cardiopulmonary resuscitation and those that received 40 min of ventricular fibrillation and unsuccessful open chest cardiopulmonary resuscitation (4.35 +/- 0.48 vs. 2.11 +/- 0.43 micrograms/mg protein; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
The use of electrically stimulated skeletal muscle to pump blood.
Electrically stimulated skeletal muscle can be used in many ways to pump blood. The important physiological characteristics of skeletal muscle for use in a cardiac assist role are presented. The force developed by a twitch and tetanic contraction are quantitated and the considerations in the choice of the stimulus applied to the innervating motor nerve are discussed. The importance of stimulus frequency and duration of the stimulus train are presented in terms of the stroke volume produced by skeletal muscle contracting around a pouch. The effect that preload has on pouch stroke volume and muscle blood flow are demonstrated. Finally an example is given in which cardiac output is augmented by an untrained, electrically stimulated, canine rectus abdominis muscle wrapped around a pouch connected between the apex of the left ventricle and the aorta. In this study, the augmentation in cardiac output was measured when the skeletal muscle was contracted after each second, third, and fourth ventricular contraction. The augmentation was 46% +/- 4, 31% +/- 7, and 25% +/- 4, respectively, for the three contraction regimens. Although electrically stimulated skeletal muscle can be used as a power source to assist the failing heart, the optimum application is yet to be discovered. Important considerations in selecting the optimal application are preload, stimulus train duration, train rate, and muscle blood flow.
Abdominal Muscles↗
The use of an electrically activated valve to control preload and provide maximal muscle blood flow with a skeletal-muscle ventricle.
A new method for optimally loading a skeletal muscle-wrapped pouch to act as a blood pump is described. The method takes advantage of the fact that the high preload pressure required for a forceful contraction needs to be present for only a short time. By using an electrically controlled valve to delay pouch filling until just before muscle contraction, pouch diastolic pressure can be kept low, which in turn maintains a high muscle capillary blood flow. The intrapouch precontraction pressure can be controlled by selecting the appropriate valve-open time (VOT). The pumping capabilities of untrained rectus abdominis and latissimus dorsi muscles were evaluated using a hydraulic circulatory system in a ten dog study (weight range 20-32.7 kg). The afterload was constant at 100 mmHg, and the pouch precontraction pressure, selected by choice of the VOT, was the test variable. It was found that for maximum pouch output, a precontraction pressure of 60-100 mmHg was required, being attained in this hydraulic model with a VOT of 400-500 msec. Typical pouch outputs were 400-600 mL/min with a muscle contraction rate of 40/min. Muscle capillary blood flow, measured with a periarterial electromagnetic flowmeter, varied inversely with pouch diastolic pressure and was near zero during tetanic muscle contraction. In one animal, a pouch output of 200 mL/min or more was maintained for more than 20 hours of continuous pumping without fatigue. In a related experiment, the method was applied to pump blood in a 32.7 kg dog, in which the muscle-wrapped pouch was connected between the descending thoracic aorta and the abdominal aorta. A pouch output of about 400 mL/min was obtained when the muscle was contracted 30 times/min and the VOT was 400 msec. This flow represented about 20% of the animal's cardiac output. This study demonstrates that by delaying pouch filling until just before the muscle is to be contracted, a low pouch diastolic pressure can be maintained, thereby maximizing muscle capillary blood flow and, in turn, providing the best opportunity for prolonged pumping.
Animals↗
Amplitude and latency characteristics of spinal cord motor-evoked potentials in dogs.
The motor-evoked potential can be reliably recorded in anesthetized dogs by use of percutaneous placement of active recording electrodes near the dorsal lamina of the vertebral column. Two types of responses were observed in this study; short (less than 5.5 ms at T9-10)- and long (greater than 5.8 ms at T9-10)-latency waves. Short-latency waves are larger in amplitude and appear with higher stimulus intensities than do long-latency waves. Short-latency waves are conducted at greater than 80 m/s and may not reflect pyramidal tract activation. The safety of using higher intensity stimuli to generate short-latency waves has not been determined.
Animals↗
Changes in expired end-tidal carbon dioxide during cardiopulmonary resuscitation in dogs: a prognostic guide for resuscitation efforts.
Expired end-tidal carbon dioxide (PCO2) measurements made during cardiopulmonary resuscitation have correlated with cardiac output and coronary perfusion pressure when wide ranges of blood flow are included. The utility of such measurements for predicting resuscitation outcome during the low flow state associated with closed chest cardiopulmonary resuscitation remains uncertain. Expired end-tidal PCO2 and coronary perfusion pressures were measured in 15 mongrel dogs undergoing 15 min of closed chest cardiopulmonary resuscitation after a 3 min period of untreated ventricular fibrillation. In six successfully resuscitated dogs, the mean expired end-tidal PCO2 was significantly higher than that in nine nonresuscitated dogs only after 14 min of cardiopulmonary resuscitation (6.2 +/- 1.2 versus 3.4 +/- 0.8 mm Hg; p less than 0.05). No differences in expired end-tidal PCO2 values were found at 2, 7 or 12 min of cardiopulmonary resuscitation. A significant decline in end-tidal PCO2 levels during the resuscitation effort was seen in the nonresuscitated group (from 6.3 +/- 0.8 to 3.4 +/- 0.8 mm Hg; p less than 0.05); the successfully resuscitated group had constant PCO2 levels throughout the 15 min of cardiac arrest (from 6.8 +/- 1.1 to 6.2 +/- 1.2 mm Hg). Changes in expired PCO2 levels during cardiopulmonary resuscitation may be a useful noninvasive predictor of successful resuscitation and survival from cardiac arrest.
Animals↗
Paired comparisons of steroid-eluting and nonsteroid endocardial pacemaker leads in dogs: electrical performance and morphologic alterations.
The effects of steroid elution from endocardial pacemaker electrodes on electrical performance and the thickness and cellularity of the reactive fibrous connective tissue formed around the stimulating electrode (peri-electrode tissue) were determined. Comparison was made with a nonsteroid electrode implanted in the same cardiac chamber (right ventricle) in each of six dogs for 6 weeks. Paired Students' t-tests showed that steroid-eluting leads had significantly (P less than .05): (1) lower voltage stimulation thresholds (as determined in sequential measurements made on the conscious animals during the experiment and on the anesthetized dogs at termination of the study); (2) less fibrous connective tissue formation around the electrode surfaces; and (3) fewer cells per unit area of peri-electrode fibrous connective tissue. There were also fewer (P less than .10) mast cells in the reactive connective tissue surrounding steroid-eluting leads. The thinner reactive connective tissue surrounding the steroid-eluting electrodes was correlated with lower voltage stimulation thresholds (r = 0.7, P less than .01). This is consistent with the hypothesis that the effect of the peri-electrode connective tissue is to increase the virtual surface area of the electrode, decreasing current density in adjacent stimulatable tissue. The relatively fewer total cells and mast cells in the peri-electrode connective tissue of the steroid-eluting electrodes suggest that the observed differences in fibrous connective tissue thickness, and therefore voltage stimulation threshold, may be related to a relatively decreased population of inflammatory cells due to the anti-inflammatory properties of the steroid.
Animals↗
Effect of adrenal function on gastrointestinal peptide release in experimental cardiac arrest.
Pancreatic polypeptide (PP), neurotensin, substance P, and vasoactive intestinal polypeptide (VIP) are peptides that modify various autonomic and neural functions. These substances are secreted into the blood in response to physiologic stimuli affecting the gastrointestinal tract. To determine the effect of adrenal hormones on gastrointestinal peptide release we measured blood levels of PP, VIP, substance P, and neurotensin in adrenalectomized and intact dogs undergoing cardiac arrest and cardiopulmonary resuscitation (CPR), a condition associated with maximal adrenal stimulation. One hour after completion of abdominal surgery consisting of bilateral adrenalectomy or exposure of the adrenal glands (sham operation), ventricular fibrillation was induced in 19 dogs by direct ventricular discharge. Despite marked elevations of plasma epinephrine and norepinephrine, CPR was associated with minimal endocrine gastrointestinal involvement, restricted to increased VIP levels in sham-operated dogs. No specific gastrointestinal peptide response to cardiac arrest was seen in adrenalectomized animals, but their plasma PP and VIP levels were higher than those of sham-operated dogs. Therefore, acute maximal adrenal stimulation is associated with selective VIP release. In addition, the higher level of the vagally controlled plasma PP in adrenalectomized animals suggests a tonic inhibitory effect of adrenal secretions on the release of this peptide.
Adrenal Glands↗
Internal ventricular defibrillation with sequential pulse countershock in pigs: comparison with single pulses and effects of pulse separation.
We compared single to sequential pulse shocks with different pulse separations on internal cardiac defibrillation by using a catheter and plaque electrodes in open-chest halothane-anesthetized pigs. Ten seconds after fibrillation onset, defibrillation was attempted using trapezoidal pulses of 65% tilt, approximately 5 ms duration and fixed outputs from 1.0 to 50 joules (J). With single pulses, minimum defibrillation energy for the catheter alone was 2.4 +/- 0.3 J/kg (mean +/- standard error) and 2.1 +/- 0.2 J/kg for the catheter tip to plaque configuration. With sequential pulse shocks, the first pulse delivered via the catheter and the second pulse from the catheter tip to the plaque electrode, the energy necessary for defibrillation was dependent on the separation time between the two pulses (2.0 +/- 0.2, 1.5 +/- 0.2, 0.9 +/- 0.1, 1.3 +/- 0.3, 0.6 +/- 0.2, and 1.2 +/- 0.2 J/kg at 100, 10, 1, 0.5, 0.2, and 0.1 ms, respectively). Further, at the 0.2 ms separation, 100% of the animals could be defibrillated with less than 2.0 J/kg (35 J total). We conclude that sequential pulse defibrillation provides a significant improvement over single pulse defibrillation. The optimum separation between the sequential pulses in this study was 0.2 ms.
Animals↗
Elevation of ventricular defibrillation threshold in dogs by antiarrhythmic drugs.
Effects of antiarrhythmic drugs upon the threshold delivered energy (TDE) and threshold peak current (TPC) for electrical ventricular defibrillation by damped sinusoidal shocks were investigated in 25 pentobarbital-anesthetized dogs. TDE and TPC were increased by the three antiarrhytmic drugs tested. Bolus injections produced a transient rise and continuous infusions produced a steady rise in difibrillation threshold. The maximal percent elevations in mean defibrillation threshold during the 60 minutes after intravenous drug treatment in groups of n = 5 dogs were: (formula: see text). Accordingly, individuals receiving antiarrhythmic drugs who nonetheless fibrillate may require greater electric shock strength for defibrillation.
Animals↗
Electrocardiographic and serum enzymic alterations associated with cardiac alterations induced in dogs by single transthoracic damped sinusoidal defibrillator shocks of various strengths.
The safety margin between the strength of shock needed to defibrillate the ventricle and shocks which produce cardiac damage has not previously been reported. This study quantitates the shock intensity required to produce ECG alterations, serum alpha-1LDH and MB CPK isoenzyme elevation and myocardial damage using single transchest damped sinusoidal defibrillator shocks. Shocks of 1 to 20 amperes per Kg. of body weight were applied. Fifty-six dog weighing 2.4 to 15 kilograms were shocked with defibrillator pulses via 10 centimeter diameter electrodes applied to the thorax. Electrocardiograms were taken to be analyzed for arrhythmias, S-T segment changes, and T wave changes. Serum enzyme levels were determined in 25 dogs. Macroscopic and histopathologic studies were conducted on the hearts. Transchest single damped sine wave shocks did not produce microscopically detectable cardiac damage until at least a threefold current overdose was applied. No macroscopic morphologic alterations were observed until at least a sixfold current overdose was applied and no deaths occurred until a twelvefold or greater current overdose was delivered. Incidence and severity of ECG changes, increase in serum enzyme activity, incidence and severity of cardiac damage, and incidence of mortality all correlated positively with shock strength. However, these four adverse effects did not correlate well with each other. Transient ECG changes were very frequent following shock application regardless of the morphologic damage produced, and hence the transient changes have little value as indicators or predictors of damage. Persistent ECG changes were predictive of morphologic changes but were not sensitive enough to detect damage in mildly injured hearts. Likewise, elevated serum cardiac isoenzyme activity was a reliable but insensitive indicator of damage.
Animals↗
Emergency defibrillation dose: recommendations and rationale.
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Adult↗