Irradiation-hyperthermia in canine hemangiopericytomas: large-animal model for therapeutic response.

Results of irradiation-hyperthermia treatment in 11 dogs with naturally occurring hemangiopericytoma were reported. Similarities of canine and human hemangiopericytomas were described. Orthovoltage X-irradiation followed by microwave-induced hyperthermia resulted in a 91% objective response rate. A statistical procedure was given to evaluate quantitatively the clinical behavior of locally invasive, nonmetastatic tumors in dogs that were undergoing therapy for control of local disease. The procedure used a small sample size and demonstrated distribution of the data on a scaled response as well as transformation of the data through classical parametric and nonparametric statistical methods. These statistical methods set confidence limits on the population mean and placed tolerance limits on a population percentage. Application of the statistical methods to human and animal clinical trials was apparent.

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.

Twenty-four hour survival in a canine model of cardiac arrest comparing three methods of manual cardiopulmonary resuscitation.

Two new modifications of manual cardiopulmonary resuscitation, high impulse compression at a rate of 120/min and interposed abdominal compression at a rate of 60/min, have been reported to produce better hemodynamic responses than standard cardiopulmonary resuscitation at 60/min. However, the effect of these two new methods on initial resuscitation success and 24 hour survival is unknown. In this study, 30 mongrel dogs were divided into three equal groups, each treated with one of three types of manual cardiopulmonary resuscitation. Ventricular fibrillation was induced electrically in morphinized, endotracheally intubated dogs emerging from halothane anesthesia. After 3 minutes of circulatory arrest without intervention, one of the three techniques of manual cardiopulmonary resuscitation was begun, and continued for 17 minutes. Defibrillation was performed at 20 minutes. Successful resuscitation was defined as a mean arterial blood pressure of at least 60 mm Hg, without chest compressions, 10 minutes after the initial defibrillation attempt. Intensive care was provided for 2 hours, including hemodynamic and respiratory monitoring, and drug intervention when required. Twenty-four hour survival and neurologic deficit were used as critical measures of outcome. Ten of 30 animals survived 24 hours with a mean neurologic deficit score of 5% (normal = 0, brain dead = 100). There was no difference in initial resuscitation success, 24 hour survival or neurologic deficit of the survivors among the three manual cardiopulmonary resuscitation methods. Aortic diastolic and calculated coronary perfusion pressures were similar for all three methods. Well performed standard manual cardiopulmonary resuscitation is as effective as these modified versions (high impulse compression and interposed abdominal compression) when compared in the same animal model.

Multicenter investigation of coronary stenting to treat acute or threatened closure after percutaneous transluminal coronary angioplasty: clinical and angiographic outcomes.

OBJECTIVES: This study reports on the initial experience with the Gianturco-Roubin flexible coronary stent. The immediate and 6-month efficacy of the device and the incidence of the complications of death, myocardial infarction, emergency coronary artery bypass surgery and recurrent ischemic events are presented. BACKGROUND: Abrupt or threatened vessel closure after coronary angioplasty is associated with increased risk of myocardial infarction, emergency coronary artery bypass graft surgery and in-hospital death. When dissection or prolapse of dilated plaque into the lumen is unresponsive to additional or prolonged balloon catheter inflation, coronary stenting offers a nonsurgical mechanical means to rapidly restore stable vessel geometry and adequate coronary blood flow. METHODS: From September 1988 through June 1991, 518 patients underwent attempted coronary stenting with the 20-mm long Gianturco-Roubin coronary stent for acute or threatened vessel closure after angioplasty. In 494 patients, one or more stents were deployed. Thirty-two percent of patients received stents for acute closure and 69% for threatened closure. RESULTS: Successful deployment was achieved in 95.4% of patients. Overall, stenting resulted in an immediate angiographic improvement in the diameter stenosis from 63 +/- 25% before stenting to 15 +/- 14% after stenting. Emergency coronary artery bypass graft surgery was required in 4.3% (21 of 493 patients). The incidence of in-hospital myocardial infarction (Q wave and non-Q wave) was 5.5% (27 of 493 patients). At 6 months, myocardial infarction was infrequent, occurring in 1.6% (8 of 493 patients). The incidence of in-hospital death was 2.2% (11 of 493 patients). Late death occurred in 7 patients (1.4%) and 34 patients (6.9%) required later bypass graft surgery. Complications included blood loss, primarily from the arterial access site, and subacute thrombosis of the stented vessel in 43 patients (8.7%). CONCLUSIONS: The early multicenter experience suggests that this stent is a useful adjunct to coronary angioplasty to prevent or minimize complications associated with flow-limiting coronary artery dissections previously correctable only by surgery. Although this study was not randomized, it demonstrated a high technical success rate and encouraging results with respect to the low incidence of emergency coronary artery bypass graft surgery and myocardial infarction.

Methylene blue as an inhibitor of superoxide generation by xanthine oxidase. A potential new drug for the attenuation of ischemia/reperfusion injury.

Tissue oxidases, especially xanthine oxidase, have been proposed as primary sources of toxic oxygen radicals in many experimental models of disease states. Among these, ischemia-reperfusion injury may be of the greatest clinical interest. In this paper we propose the use of methylene blue as a means of suppressing the production of superoxide radicals O2- by acting as an alternative electron acceptor for xanthine oxidase. Previous work has indicated that methylene blue accepts electrons from xanthine oxidase at the iron-sulfur center. Initial experiments in our laboratory demonstrated that (1) pairs of electrons from each enzymatic oxidation are transferred to methylene blue, (2) the reduction of methylene blue can be achieved by model iron-sulfur centers, similar to the iron-sulfur center of xanthine oxidase, (3) reduced methylene blue auto-oxidizes to produce H2O2 directly, rather than O2-, and (4) methylene blue is effective at non-toxic levels (2-5 mg/kg) in preventing free radical damage to liver and kidney tissues in an in vitro model of ischemia and reoxygenation. Accordingly, we propose that methylene blue may represent a new class of antioxidant drugs that competitively inhibit reduction of molecular oxygen to superoxide by acting as alternative electron acceptors for tissue oxidases. We have termed these agents "parasitic" electron acceptors.

The safety factor for electroventilation measured by production of cardiac ectopy in the anesthetized dog.

The safety factor of electroventilation (ie, the ratio of the current required to produce an ectopic beat to the current required to produce an inspired volume of 225 ml, which is approximately twice tidal volume) was determined in 12 pentobarbital-anesthetized dogs using transthoracic electrodes positioned at the optimal electroventilation site. The optimal stimulation site for electroventilation was first determined using hand-held, stimulating electrodes. Then electrodes, 4.1 cm in diameter, were sutured bilaterally to the optimal stimulation site. The relationship between inspired volume and stimulus intensity was determined using a 0.8-s burst of stimuli (60/s) with a pulse duration of 0.1 ms. Using the same electrodes, the threshold current for producing ectopic beats was determined for single pulses ranging from 0.1 to 10 ms duration. In all dogs, the current required to produce an ectopic beat increased greatly as the pulse duration decreased. At 0.1 ms, the safety factor for electroventilation was calculated to be 25.8.

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.

The relationship of carbon dioxide excretion during cardiopulmonary resuscitation to regional blood flow and survival.

Currently, there are no practical means of prospectively determining cardiopulmonary resuscitation (CPR) adequacy in the field. Airway CO2 excretion can be noninvasively and stably measured under changing environmental conditions. We investigated the relationships between the volume of airway CO2 excreted (CO2EX) during CPR to regional blood flow (RBF) and survival. A total of 21 dogs were randomly divided into four CO2EX groups (< 5, 5-6, > 6-7 and > 7 ml CO2/min per kg), anesthetized, instrumented and ventilated with an in-line infrared airway CO2 sensor. Anesthesia was reduced and baseline measurements made. Ventricular fibrillation (VF) was initiated and resuscitation withheld for 3 min, followed by 17 min of CPR. Compression force alone was adjusted to maintain predetermined CO2EX. Animals were resuscitated, monitored for 2 h and observed for an additional 22 h. RBF was determined at baseline, 16 min post-VF and 60 min post-resuscitation. Mean CO2EX during CPR was significantly higher in survivors than nonsurvivors. The probability of survival increased as CO2EX increased. The highest CO2EX group had the highest rate of survival (86%), but did not always have significantly higher cardiac output (CO), myocardial or cerebral blood flows (MBF, CBF) than the lowest CO2EX group with a 0% survival rate. These data suggest survival is tracked better by CO2EX than by CO, MBF or CBF. Therefore, CO2EX appears to provide a practical reliable noninvasive method of determining CPR efficacy in the field.

The relationship between airway carbon dioxide excretion and cardiac output during cardiopulmonary resuscitation.

There is currently no practical method for determining cardiopulmonary resuscitation (CPR) efficacy in the field. We investigated the relationship between the volume of carbon dioxide (CO2) excreted in the airway (CO2EX) when tidal volume and respiratory rate are controlled, and cardiac output (CO), an indicator of CPR efficacy, to determine the potential of CO2EX as a practical noninvasive field monitor of CPR efficacy. Thirteen mongrel dogs were anesthetized, instrumented and ventilated 13 times/min at a fixed tidal volume with an infrared airway CO2 sensor. CO2EX = (PCO2/bar. press) x (tidal vol) x (breaths/min), and expressed in ml/min per kg. Sequences of control, CPR with 3-4 different compression forces, and recovery measurements were recorded 10-15 times/animal. CO2EX and CO fell simultaneously with ventricular fibrillation. CPR immediately increased CO2EX and CO. Both changed consistently and in the same direction as compression force. Return of spontaneous circulation immediately increased CO2EX and CO above controls, with a gradual return to control levels. CO2EX was always below 8 ml-CO2/min/kg during CPR and above this during spontaneous circulation. With alveolar ventilation controlled, CO2 movement is regulated by CO, CO distribution and CO2 stores shifts. Normally, CO accounts for 15% of CO2EX variability. In this study CO accounted for > or = 65% of CO2EX variability during CPR, indicating CO2EX changes were primarily due to CO changes. When ventilation is controlled, CO2EX during CPR reliably tracks changes in CO. Therefore, CO2EX may provide a practical noninvasive method of determining CPR efficacy as the CPR is being performed.

The effectiveness of postischemic oxypurinol administration upon myocardial function in the isolated rat heart.

The Langendorff isolated rat heart preparation was used to determine the effect of oxypurinol, a xanthine oxidase inhibitor, on myocardial function when administered during reperfusion after 30 min of warm ischemia. Twenty rats were randomly sorted into 2 groups of 10, and an isolated heart preparation made from each rat. The isolated hearts were perfused for 15 min with a modified Krebs-Henseleit solution to permit stabilization of the preparation. Each heart was then subjected to 30 min of total ischemia at 37 degrees C followed by 40 min of reperfusion with either saline-treated perfusate or oxypurinol-treated perfusate (1.3 mM). The maximum power produced and the preload required to produce maximum power were both determined prior to ischemia and every 10 min after ischemia during 40 min of reperfusion. The saline-treated group, but not the oxypurinol-treated group, showed significantly less maximum power output at all testing times during reperfusion compared to the preischemic value (P less than 0.05). There was a significantly greater maximum power output (P less than 0.02) in the oxypurinol-treated group compared to the saline-treated group after 20, 30, and 40 min of reperfusion. There were no differences within either group, or between groups, for the preload required to produce maximum power at any of the testing times. Ultrastructural examination of myocardium after reperfusion showed severe mitochondrial and myofibrillar disruption in the saline-treated group but not in the oxypurinol-treated group. We conclude that oxypurinol administered following 30 min of total ischemia at the onset of reperfusion, can preserve myocardial function during the early reperfusion period in the isolated rat heart.

Fluid loading with whole blood or Ringer's lactate solution during CPR in dogs.

The influence of fluid loading during CPR on oxygen uptake and blood flow was investigated in 18 dogs (12-26 kg). Blood flows were measured with radioactive microspheres at 5 (control CPR), 13 and 20 min after the initiation of ventricular fibrillation and CPR. After 10 min, 9 dogs received a rapid infusion of whole blood (11 ml/kg, i.v.) and 9 dogs received Ringer's solution (11 ml/kg, i.v.). Oxygen uptake was not significantly altered by fluid loading with either whole blood or Ringer's solution. Fluid loading increased cardiac output 34% over the 5 min control value. However, left ventricular perfusion decreased to 74% and brain flow decreased to 65% of control. At 20 min, cardiac output and brain flow returned to near control values, while left ventricular flow remained low. Changes in organ perfusion can be explained in part by the concurrent changes in blood pressures. Central venous diastolic pressure increased significantly (from 9 to 14 mmHg) after fluid load. However, central arterial diastolic pressure did not rise proportionately (from 32 to 34 mmHg). Hence, the central A-V diastolic pressure difference decreased. Although fluid loading during CPR improved cardiac output, flow to the heart and brain decreased. Further, there was no increase in oxygen consumption, indicating that fluid loading did not improve metabolic status.

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.

Neurologic outcome following successful cardiopulmonary resuscitation in dogs.

Successful cardiopulmonary resuscitation necessitates that both myocardial and central nervous system function be restored with minimal long-term damage. Recent resuscitation research has emphasized minimizing neurologic damage during and after cardiopulmonary resuscitation. However, whether neurologic damage is a major cause of death or morbidity following successful cardiopulmonary resuscitation is unknown. This study examined the role of neurologic injury as a cause for morbidity and mortality following cardiopulmonary resuscitation, and if parameters used successfully during resuscitation for assessing the potential for myocardial salvage, could also be used to predict neurologic outcome. Eighty-eight mongrel dogs underwent 3 min of untreated ventricular fibrillation and either 15 or 17 min of cardiopulmonary resuscitation. Twenty-four hour survivors were evaluated with a neurologic deficit scoring system. Thirty-one percent of these animals were never resuscitated. Twenty-eight percent were resuscitated, but expired prior to 24 h. Approximately half of those who expired after resuscitation died from apparent neurologic sequellae. Forty-one percent of the 88 animals survived for 24 h. Two-thirds of these survivors were completely neurologically normal, while one-third were neurologically impaired. Hemodynamic parameters useful in assessing cardiovascular prognosis were not helpful in predicting neurologic outcome. Hence, although the majority of resuscitated animals did not suffer neurologic damage, up to one-third did exhibit neurologic impairment following resuscitation. Neurologic injury is also a major contributor to early death following successful resuscitation. Hemodynamic parameters of cardiovascular recovery do not predict neurologic outcome after prolonged cardiopulmonary resuscitation.

Continuous monitoring of cerebral perfusion by thermal clearance.

Currently, no commercially available system exists to continuously monitor the effective tissue perfusion within the parenchyma of the brain. While several methods exist for accurately measuring cerebral perfusion; among them: 133xeonon clearance, hydrogen clearance and radiolabeled microsphere injection; none of these methods provides continuous monitoring. The Cook Incorporated VH8500 Volumetric Hyperthermia Treatment System (Bloomington, IN, USA) was initially developed to treat brain tumours by maintaining constant, moderate hyperthermia within a defined tissue volume over an extended duration. The system continuously adjusts the power applied to heating elements in order to maintain a constant temperature within the treatment volume. Because tissue perfusion is a primary factor responsible for removing heat from tissue, monitoring the amount of power applied to the heating elements allows one to continuously estimate tissue perfusion in the vicinity of the heating elements. In the current study, regional blood flow in the vicinity of heater/sensor catheters implanted in the brain parenchyma of three dogs was estimated by the VH8500 tissue perfusion algorithm and directly measured with radioactive labeled microspheres. The accuracy of the perfusion estimate (Thermal Perfusion Index) was evaluated by comparing these values. A range of blood flow was achieved in each animal by infusing nitroprusside. It was found that with the perfusion estimation algorithm of the Cook Incorporated VH8500 Volumetric Hyperthermia Treatment System as it is currently implemented, the Thermal Perfusion Index tended to underestimate regional perfusion as measured with radioactive microspheres, but the relationship was nearly linear. Thus, the system currently tracks changes in regional blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

The chronaxie for myocardium and motor nerve in the dog with chest-surface electrodes.

The chronaxie (i.e., the duration for a stimulating current having twice the rheobasic, or minimum, value) was determined for ventricular myocardium in 12 pentobarbital-anesthetized dogs. Current was applied transthoracically via chest-surface electrodes located at the optimal axillary site for producing inspiration by stimulation of the phrenic nerve (electroventilation). In four dogs the chronaxie for motor-nerve was determined using electrodes at the same location. After using hand-held electrodes to identify the optimal stimulation site for electroventilation, 4.1 cm diameter electrodes were applied bilaterally to the optimal site on the thorax. In 12 dogs, the threshold current for producing ventricular ectopic beats was determined for single rectangular current pulses ranging from 0.1-10 ms in duration. From these data, strength-duration curves were determined and the average chronaxie for ventricular myocardium was found to be 1.82 ms. In four dogs the relationship between inspired volume and maximum stimulus intensity was determined using a 0.8 s burst of stimuli (60/s) with pulse durations ranging from 20-500 microseconds. From these data, strength-duration curves for current were constructed and the average chronaxie for motor-nerve was found to be 0.17 ms. The results of this study show that, because of the differing chronaxies, the current required to produce inspiration with short-duration stimuli is much less than that required to evoke an ectopic heart beat.

An acoustical guidance and position monitoring system for endotracheal tubes.

A prototype instrument to guide the placement and continuously monitor the position of an endotracheal tube (ETT) was developed. An incident audible sound pulse is introduced into the proximal ETT and detected as it travels down the ETT via a miniature microphone located in the wall. This pulse is then emitted from the tube tip into the airways and the reflected signal from the airways is detected by the microphone. A well defined reflection arises from the point where the total cross sectional area of the airways increases rapidly, and the difference in timing between detection of the incident pulse and this reflection is used to determine ETT position or movement. This reflection is not observed if the ETT is erroneously placed in the esophagus. The amplitude and polarity of an additional reflection that occurs at the ETT tip is used to estimate the cross-sectional area of the airway in which the ETT is placed. This combined information allows discrimination between tracheal and bronchial intubation and can be used to insure an adequate fit between the ETT and trachea. The instrument has proven extremely reliable in multiple intubations in eight canines and offers the potential to noninvasively and inexpensively monitor ETT position in a continuous manner.

Cardiac assistance with electrically stimulated skeletal muscle.

This study examined the ability of a skeletal muscle-powered assist ventricle (SMV) to augment cardiac output in ten dogs with pharmacologically induced heart failure under acute conditions. An SMV was surgically constructed in each dog by wrapping the untrained rectus abdominis muscle around a compressible pouch that was inserted into a left ventricular apex-to-aortic vascular conduit. The multiple motor nerves to the rectus muscle were then stimulated during ventricular diastole at a rate which equalled a ratio of 1:2, 1:3, or 1:4 with the natural ventricular beat. There was an increased cardiac output during SMV assistance compared with preassistance values in all ten dogs at each stimulation ratio with a mean increase of 46 +/- 4 per cent with a ratio of 1:2, 25 +/- 4 per cent with a ratio of 1:3, and 31 +/- 7 per cent with a ratio of 1:4 (p less than 0.01 for all values). The diastolic blood pressure and mean blood pressure were both increased (p less than 0.01 and p less than 0.05, respectively) during SMV stimulation at ratios of 1:2 and 1:3, but not 1:4. We have shown that untrained rectus abdominis muscle, when used as the power supply for a SMV in an apico-aortic conduit, can temporarily augment cardiac output in dogs with pharmacologically induced heart failure.

Impedance cardiography by use of a spot-electrode array to track changes in cardiac output in anesthetized dogs.

Transthoracic impedance cardiography is a noninvasive method to determine changes in cardiac output on the basis of the cardiac-induced impedance change measured across the thorax. In this report, we describe a new, easily applied, tetrapolar spot-electrode configuration for use in canine transthoracic impedance cardiography. The array is a convenient alternative to use of the traditional circumferential band-electrode array which, in the dog, is prohibitive because of the extensive skin preparation required. The spot-electrode array was used to compare changes in cardiac output measured by transthoracic impedance cardiography, with changes measured by a reference indicator-dilution technique. A spot-electrode array, composed of 4 standard ECG electrodes, was used to measure transthoracic impedance in 10 anesthetized dogs. Variations in cardiac output were produced by controlled hemorrhage (200- to 250-ml increments). Simultaneous reference measurements of cardiac output were made before hemorrhage (control) and at each level of hemorrhage, using the saline-dilution method. The beat-by-beat impedance changes were measured by use of a Minnesota impedance cardiograph, which also recorded the first derivative of impedance (dZ/dt). An index of cardiac output was defined as the product of the maximal value of the first time derivative of impedance, ejection time, and heart rate for each beat during inscription of a saline-dilution curve. The average of the beat-by-beat indices was calculated and then normalized relative to the initial control value. Linear regression analysis was performed to evaluate the correlation of the index of cardiac output with the reference cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Artificial respiration in the anesthetized horse using bilateral, percutaneous, cervical phrenic-nerve stimulation with needle electrodes: a preliminary report.

In this preliminary study, artificial respiration was produced in four anesthetized horses using trains of stimuli applied to long needle electrodes inserted bilaterally at the base of the neck. The needles were insulated to within 1 cm of the tips. The frequency of the stimuli (0.1 msec) was 35/sec and the train duration (duration of inspiration) was 1 sec. Inspired volume increased with increasing stimulus intensity. In two animals, inspired volumes of 6 liters were achieved. In another animal 4.5 liters was achieved and in another, 2.5 liters. This lower value probably represented less-than-optimal electrode placement. Artificial percutaneous electrophrenic respiration was maintained for half an hour in every animal using a minute volume equivalent to that when breathing spontaneously.