Direct noninvasive monitoring of spinal cord motor function during thoracic aortic occlusion.
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Animals↗
Biomedical subjects
W A Tacker
Publications and source records attributed to W A Tacker.
Plasma catecholamines and resuscitation from prolonged cardiac arrest.
Plasma catecholamine levels rise markedly with cardiac arrest and attempted resuscitation. We examined whether epinephrine (EPI) or norepinephrine (NE) plasma concentrations could predict resuscitation outcome. In nine mongrel dogs, EPI and NE levels were drawn before cardiac arrest and after 8 and 14 min of cardiac arrest and CPR. Intravenous EPI (1 mg) was given 1 min before the last plasma level was drawn. Catecholamines were quantitated by high-performance liquid chromatography with triple-electrode coulometric electrochemical detection. Plasma catecholamines increased significantly with cardiac arrest, EPI levels increased from a control level of 15.9 +/- 3.0 to 396.0 +/- 63.3 pmol/ml after 8 min of cardiac arrest (p less than .05), and NE levels similarly increased from 4.4 +/- 1.7 to 66.5 +/- 12.0 pmol/ml (p less than .01). Neither the absolute catecholamine plasma concentration nor the response to cardiac arrest of the endogenous catecholamine concentrations could predict outcome, but catecholamine responses to exogenous EPI did correlate with outcome. Animals which were subsequently resuscitated had a greater increase in the plasma EPI concentrations after exogenous EPI than animals that were not resuscitated, a 53-fold vs. a 23-fold increase (p less than .05). Successfully resuscitated animals also had increased NE levels after exogenous EPI, while unsuccessfully resuscitated animals had either no change or a decrease (p less than .02). Successfully resuscitated animals had an increase in coronary perfusion pressure (p less than .01) in response to exogenous EPI, in contrast to those that were not resuscitated. This suggests that the exogenous administration of EPI during prolonged CPR is beneficial despite markedly elevated endogenous catecholamine levels.
Animals↗
Aortic and right atrial systolic pressures during cardiopulmonary resuscitation: a potential indicator of the mechanism of blood flow.
The absolute difference between aortic and right atrial systolic pressure (systolic pressure gradient) and the difference between the aortic diastolic and right atrial diastolic pressure (coronary perfusion pressure) were evaluated in a series of 63 adult mongrel dogs undergoing five different methods of cardiopulmonary resuscitation (CPR). Fluid-filled pressure monitoring catheters were placed in the ascending aorta and right atrium in each of the animals after induction of anesthesia with morphine sulfate and 1% halothane and oxygen. The animals were then fibrillated with a transvenous electrode catheter that had been introduced into a ventricle. After a "down time" of 3 minutes during which no CPR was performed, the animals' lungs were ventilated, and one of five methods of CPR was initiated. The systolic pressure gradient and coronary perfusion pressure were measured in all animals 1 minute after CPR was begun, and in all but the group undergoing open-chest cardiac massage after 7 minutes and 17 minutes of CPR. The systolic pressure gradient and coronary perfusion pressure were greatest during open-chest cardiac massage (true cardiac compression), intermediate in external mechanical CPR (Thumper) and standard CPR (greater in small dogs than large dogs), and lowest in CPR performed with a combined thoracic and abdominal vest apparatus (predominantly thoracic pump). The observation that the systolic pressure gradient between intrathoracic chambers is largest in open-chest cardiac massage and smallest in vest CPR suggests that similar measurements recorded during the performance of human cardiac resuscitation may be useful in determining the mechanism of blood flow.
Animals↗
Myocardial perfusion pressure: a predictor of 24-hour survival during prolonged cardiac arrest in dogs.
Myocardial perfusion pressure, defined as the aortic diastolic pressure minus the right atrial diastolic pressure, correlates with coronary blood flow during cardiopulmonary resuscitation (CPR) and predicts initial resuscitation success. Whether this hemodynamic parameter can predict 24-h survival is not known. We examined the relationship between myocardial perfusion pressure and 24-h survival in 60 dogs that underwent prolonged (20 min) ventricular fibrillation and CPR. Forty-two (70%) animals were initially resuscitated and 20 (33%) survived for 24 h. Myocardial perfusion pressure was significantly greater when measured at 5, 10, 15 and 20 min of ventricular fibrillation in the resuscitated animals than in the non-resuscitated animals (P less than 0.01). Likewise, the myocardial perfusion pressure was also greater in the animals that survived 24 h than in animals that were resuscitated, but died before 24 h (P less than 0.02). Myocardial perfusion pressure measured after 10 min of CPR was 11 +/- 2 mmHg in animals never resuscitated, 20 +/- 3 mmHg in those resuscitated that died before 24 h and 29 +/- 2 mmHg in those that survived 24 h (P less than 0.05). A myocardial perfusion pressure at 10 min of CPR of 20 mmHg or less is an excellent predictor of poor survival (negative predictive value = 96%). Myocardial perfusion pressure is a useful index of CPR effectiveness and therefore may be a useful guide in helping to optimize resuscitation efforts.
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↗
Comparison of mechanical techniques of cardiopulmonary resuscitation: survival and neurologic outcome in dogs.
Three currently available mechanical devices for cardiopulmonary resuscitation (CPR) were compared using a canine cardiac arrest model. Twenty-four-hour survival without neurologic deficit was the goal. A group of 30 large mongrel dogs was divided equally among Thumper CPR, simultaneous compression and ventilation (SCV) CPR, and vest CPR. Ventricular fibrillation was induced electrically, and after 3 minutes of no intervention, one of the three types of mechanical CPR was performed for 17 minutes. SCV CPR and vest CPR produced significantly greater aortic and right atrial systolic pressures than Thumper CPR (P less than .03). The SCV CPR technique also produced significantly higher aortic diastolic pressure and right atrial diastolic pressure than either of the other methods (P less than .03). However, coronary perfusion pressure was not different among the three mechanical methods. No differences in immediate resuscitation, 24-hour survival, or neurologic deficit scores at 24 hours were found. Neither SCV nor the vest techniques of CPR appear better for survival or neurologic outcome than standard cardiopulmonary resuscitation performed with the Thumper.
Animals↗
Effects of naloxone on the adrenomedullary response during and after cardiopulmonary resuscitation in dogs.
To determine the effects of naloxone, an opiate antagonist, on the adrenomedullary response to cardiac arrest, plasma epinephrine and norepinephrine levels were measured before, during, and after cardiac arrest in dogs. Ventricular fibrillation was induced in 12 dogs anesthetized with pentobarital sodium (30 mg/kg) and standard American Heart Association cardiopulmonary resuscitation (CPR) was begun using a mechanical device. At 6.5 minutes of CPR, naloxone (10 mg/kg) or 0.9% saline (10 ml) was given intravenously. At 12 minutes of CPR, the cardiac ventricles were electrically defibrillated. Plasma epinephrine and norepinephrine levels were measured before ventricular fibrillation; at 2.5, 4.5, 9.5, and 11.5, minutes of CPR; and at 5, 10, 15, and 20 minutes after resuscitation. Epinephrine and norepinephrine increased from prearrest levels of 3.66 +/- 0.67 (+/- SE) and 24.02 +/- 3.67 ng/ml to 66.67 +/- 9.65 and 74.00 +/- 9.91 ng/ml, respectively, at 4.5 minutes of CPR. After resuscitation, norepinephrine levels remained slightly elevated, while epinephrine fell to prearrest levels. Naloxone did not cause a significant change in either epinephrine or norepinephrine from 6.5 minutes of CPR (time of treatment) through 20 minutes postresuscitation. In addition, naloxone had no effect on either the end-diastolic pressure difference during CPR or resuscitation outcome. We conclude that cardiac arrest causes significant increases in plasma epinephrine and norepinephrine levels, which remain elevated for the duration of the arrest, and that naloxone has no effect on these levels.
Adrenal Medulla↗
Motor evoked potentials in the dog: effects of global ischemia on spinal cord and peripheral nerve signals.
Motor evoked potentials (MEPs) in cats, rats, and humans have been reported. They appear promising as a test of central nervous system function, and they are sensitive not only to mechanical injury but also to ischemia. In mechanical trauma, the peripheral nerve response is much more sensitive to damage than the cord response, with a lower threshold and an earlier disappearance. We are reporting that the MEP can also be produced in the dog and that, under conditions of cardiac arrest induced by fibrillation, the peripheral nerve response disappears first at about 30 seconds and then the spinal cord response disappears at about 10 to 13 minutes. The late disappearance of the spinal cord response raises serious questions about its role as an adequate injury monitor. The most useful warning feature of the spinal cord response is an increase in amplitude during the critical first 2 minutes of arrest. Latency changes in the cord and peripheral nerve response did not seem as useful as amplitude changes in terms of providing adequate detection of injury. We also evaluated the peripheral nerve signals to determine whether they are partially volume-conducted weak muscle responses, and evidence substantiates their nonmuscle origin.
Animals↗
Choice of anesthetics for MEP studies.
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Anesthesia↗
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↗
Cerebrospinal fluid changes in experimental cardiac arrest (maximal stress).
Cardiac arrest produces a prompt and maximal increase of plasma catecholamines, with associated elevations of the hormones involved in the endocrine response to stress. To investigate the participation of the central nervous system (CNS) in the generation of the endocrine response, the catecholamines epinephrine and norepinephrine in cerebrospinal fluid (CSF) were measured before, during, and after cardiac arrest accompanied by cardiopulmonary resuscitation (CPR) in adrenalectomized (ADX) and sham-operated (SHAM) dogs. We also determined the activity of acetylcholine esterase (AChE), an intracellular enzyme released into the CSF after hypothalamic or caudate stimulation. During CPR, plasma epinephrine increased significantly in SHAM but not ADX dogs, increasing from (mean +/- SE) 480 +/- 171 to 29,800 +/- 14,200 pg/ml (P less than 0.05). Prearrest CSF norepinephrine was higher in ADX than SHAM dogs and increased in both groups with cardiac arrest, but the increase was significant only in SHAM animals; CSF epinephrine remained unchanged during or after cardiac arrest. CSF AChE activity increased during and after defibrillation; the difference with basal levels became significant when the peak postarrest values were considered (P less than 0.05). These results document biochemical changes occurring in the CNS during maximal stress represented by cardiac arrest. It is suggested that CSF norepinephrine and AChE activity elevations are markers for hypothalamic activation from the stress of cardiac arrest.
Acetylcholinesterase↗
Plasma catecholamine and serum cortisol responses to experimental cardiac arrest in dogs.
The plasma catecholamine and serum cortisol responses to cardiac arrest (ventricular fibrillation), cardiopulmonary resuscitation (CPR), and ventricular defibrillation were examined in 10 intact (sham-operated controls) and 10 bilaterally adrenalectomized dogs. One hour after surgery, the cardiac ventricles were electrically fibrillated, and 30 s later Standard American Heart Association CPR was begun. After 12 min of CPR, the ventricles were defibrillated. Cardiac arrest per se results in a massive increase in plasma epinephrine and norepinephrine concentrations and indicates that the adrenal medullas are the predominant source of this response. Although the epinephrine response was virtually nonexistent in the adrenalectomized dogs, the norepinephrine response was approximately 30% of that in the sham-operated control animals. Thus there is an adrenomedullary, and perhaps a sympathetic neural, component to the sympathochromaffin response to cardiac arrest. Resuscitation from experimental cardiac arrest tended (P greater than 0.05 less than 0.1) to be lower in the adrenalectomized dogs (1 of 10) than in the animals with intact adrenal glands (6 of 10).
Animals↗
Long-term survival with open-chest cardiac massage after ineffective closed-chest compression in a canine preparation.
The ultimate goal of cardiopulmonary resuscitation (CPR) is long-term, neurologically intact survival. This study examined whether open-chest cardiac massage could improve 7 day survival and neurologic function when instituted after the failure of standard closed-chest compression CPR. Twenty-nine mongrel dogs were anesthetized and then instrumented with catheters to monitor right atrial and ascending aortic pressures. Ventricular fibrillation was induced and after 3 min standard CPR was begun. Standard CPR was performed with a Thumper programmed for 2 inch chest compressions at 60/min with a 50% duty cycle. External defibrillation was attempted twice after 15 min of ventricular fibrillation. Unsuccessfully defibrillated animals were randomly assigned to either an additional 2 min of continued closed-chest compressions, or 2 min of open-chest cardiac massage. All animals underwent a period of advanced cardiac life support and were followed until they were resuscitated or died. Follow-up care, including scoring of neurologic deficit, was performed for 7 days. In dogs receiving open-chest cardiac massage there was significantly more immediate resuscitation success (14/14 vs 5/14; p less than .005), 24 hr survival (12/14 vs 4/14; p less than .005), and 7 day survival (11/14 vs 4/14; p less than .02) than in those receiving continued closed-chest compression. Open-chest cardiac massage significantly improved long-term outcome when instituted after 15 min of ineffective closed-chest compression.
Animals↗
Induction and prevention of acceleration atelectasis.
Acceleration atelectasis is the absorptional collapse of alveoli in the dependent lung due to increased accelerative forces. It is exacerbated by breathing 100% oxygen and, during +Gz exposure, by the use of an anti-G suit. Experiments were conducted on 12 subjects using simulated aerial combat maneuvers (SACM) with G profiles having peak exposures of either 4.5 G or 9 G. Decreases in vital capacity (VC) measurements were used as quantification of atelectasis, two types of reduction being identified and described. Labile reductions in VC were readily restored by a deep breath or cough. Such reduction approximated 28% following the 4.5-G SACM and 25% following the 9-G SACM. More persistent (so called) stable reductions were of lesser degree, values of -20% being seen following both 9 G and 4.5 G maneuvers. Acceleration atelectasis causes symptoms of chest pain, coughing, and shortness of breath. Subjective ratings of the severity of these symptoms were obtained from the subjects, and these were much greater following the 4.5-G SACM exposures than after the 9-G runs. Acceleration atelectasis was reduced by dilution of the inspired oxygen concentration by argon and nitrogen (evaluated at 95, 82.5, 70, 50, and 20% oxygen); the addition of unassisted positive pressure at 30 mm Hg (4 kPa) to the breathing mask; or the performance of the anti-G straining maneuver (AGSM).
Acceleration↗
Comparison of the efficacy of defibrillation with the damped sine and constant-tilt current waveforms in the intact animal.
The efficacy of defibrillation using the damped sine and constant-tile (60%) truncated exponential waveforms was determined in each of nine dogs. Two measures of efficacy were used to compare the two waveforms: 1) threshold defibrillation current and 2) percent successful defibrillation. For both measures of efficacy, shock strength was expressed in terms of delivered energy. Mean threshold energy was 0.98 J/kg for the damped sine wave and it was 1.24 J/kg for the truncated exponential waveform. Percent successful defibrillation versus energy/kg curves were constructed for each of the waveforms and were found to be essentially the same. Percent successful defibrillation increased with increasing shock intensity. For 50% success, the energy for the damped sine wave was 1.16 J/kg; for the truncated exponential wave, the corresponding value was 1.15 J/kg. A shock of threshold intensity successfully defibrillated in approximately 50% of the defibrillation attempts, i.e., defibrillation threshold corresponds to about 50% successful defibrillation.
Animals↗
Sequential pulse defibrillation in man: comparison of thresholds in normal subjects and those with cardiac disease.
We compared the parameters describing the defibrillation threshold in patients with normal hearts and in patients with ischemic heart disease, using a special electrode system and sequential pulses of current. Twenty-eight patients consented to the study (mean age: 36.6 +/- 10.1 years; mean mass: 80.7 +/- 13.8 kg). Twenty-one patients underwent surgery for Wolff-Parkinson-White syndrome (relatively normal hearts). Six patients had a history of previous myocardial infarction and aneurysm or coronary artery disease; and one patient had been resuscitated from an episode of sudden death, without evidence of consequent myocardial damage. For 26 patients, defibrillation thresholds were determined intraoperatively by passing sequential pulses through a catheter electrode and epicardial mesh electrode. For 2 patients defibrillation thresholds were determined during electrophysiologic study, after ventricular fibrillation was induced by programmed stimulation, by passing sequential pulses through a catheter and skin-patch electrode. Parameters for sequential pulse defibrillation thresholds between the two groups did not differ appreciably. Total energy for patients with normal hearts averaged 9.9 +/- 6.3 J compared to 8.9 +/- 4.6 J for patients with cardiac disease. No patient with cardiac disease had defibrillation parameters that exceeded the range of the normal patients. These results suggest that the presence of cardiac disease may not significantly alter the parameters necessary for successful defibrillation when using sequential pulses for delivery of energy.
Adult↗
The comparative pathology of open chest vs. mechanical closed chest cardiopulmonary resuscitation in dogs.
We compared the pathologic changes following open-chest cardiopulmonary resuscitation (OCCPR) vs. closed chest cardiopulmonary resuscitation (CCCPR) in 28 healthy mongrel dogs subjected to experimentally induced ventricular fibrillation (VF). VF was induced in 29 dogs. No treatment was given for 3 min, then mechanical CCCPR was given for the next 12 min. External defibrillation (80 joules) was then attempted twice. One dog was resuscitated. The remaining 28 dogs were divided into 2 groups of 14 each. Group A received continued CCCPR and group B received OCCPR. All dogs received advanced cardiac life support and were followed until resuscitated or dead. All dogs were autopsied and gross pathology scores and histopathology scores were determined for each animal, and for each of 19 separate tissues within each animal. The mean gross pathology scores for the following tissues were significantly greater for dogs that received OCCPR vs. those that received CCCPR: skin (3.4 vs. 1.2; P less than 0.001), subcutaneous tissue (3.7 vs. 0.6; P less than 0.001), chest wall muscle (3.7 vs. 0.5; P less than 0.001), and pleura (1.9 vs. 0.1; P less than 0.001). The mean total gross pathology score was also greater in dogs that received OCCPR vs. those that received CCCPR (17.2 vs. 7.7; P less than 0.001). The mean histopathology scores for the following tissues were significantly greater for dogs that received OCCPR vs. those that received CCCPR: skin (2.5 vs. 0.0; P less than 0.001), subcutaneous tissue (2.2 vs. 0.1; P less than 0.001), muscle (2.3 vs. 0.1; P less than 0.001), pleura (1.6 vs. 0.0; P less than 0.001), pericardium (1.4 vs. 0.2; P less than 0.01), epicardium (2.5 vs. 0.2; P less than 0.001), myocardium (2.5 vs. 0.3; P less than 0.001), and endocardium (1.9 vs. 0.5; P less than 0.01). The mean total histopathology score was also greater in dogs that received OCCPR vs. those that received CCCPR (20.1 vs. 7.4; P less than 0.001). The histopathology score for brain tissue was greater for the CCCPR group than for the OCCPR group (1.9 vs. 0.4; P less than 0.05). This study showed that OCCPR in dogs following VF caused more severe pathologic changes than CCCPR. These changes were attributed to thoracotomy-induced chest wall injury and to internal defibrillation induced myocardial injury. However, OCCPR caused less severe microscopic brain lesions than CCCPR.
Animals↗