Garfield B. Russell

Reliability of the arterial to end-tidal carbon dioxide gradient in mechanically ventilated patients with multisystem trauma

The accuracy and reliability of the relationship between arterial and end-tidal carbon dioxide (PETCO2 and PaCO2), expressed as the gradient, P(a-ET)CO2, was assessed with 171 comparisons in nine mechanically ventilated trauma patients. The P(a-ET)CO2 was 14 +/- 11 mm Hg. (mean +/- standard deviation.) The positive correlation between PaCO2 (44 +/- 10 mm Hg) and PETCO2 (30 +/- 10 mm Hg) for the study population (reflected by r = 0.64, p = 0.001; but r2 = 0.41) indicated statistical significance, but only 40% of the changes reflected a linear relationship. Seventy-eight percent of individual patients had significant correlations of PaCO2 and PETCO2 (p < 0.02 to p < 0.001). Changes in PETCO2 erroneously predicted the PaCO2 changes in 27% of comparisons with 15% false decreases and 12% false increases. Trends in P(a - ET)CO2 magnitude are not reliable, and concordant direction changes in PETCO2 and PaCO2 are not assured.

Stability of arterial to end-tidal carbon dioxide gradients during postoperative cardiorespiratory support.

The changes in the arterial to endtidal carbon dioxide gradient, P(a-ET)CO2, were studied in postoperative cardiac surgery patients from the time of admission to the intensive care unit, during changing cardiorespiratory support, up to the time of tracheal extubation. Individual factors evaluated for their effects on P(a-ET)CO2 included rate of mechanical ventilation, infusion of vasoactive agents (nitroglycerin, nitroprusside, dopamine, dobutamine, and metariminol), and associated changes in haemodynamic pathophysiology (cardiac index, pulmonary artery pressure, pulmonary vascular resistance index, systemic vascular resistance index, and pulmonary capillary wedge pressure). After approval by the Clinical Investigation Committee, 59 patients, age 63 ± 9(41 to 75) yr, were studied and 382 individual gradient determinations made. Mean P(a-et)CO2 was 5.47 ± 5.21 mmHg, with the mean PaCO2, 36.51 ± 5.89 mmHg and meanetCO2, 31.04 ± 6.44 mmHg. For the population as a whole, the correlation between PaCO2 andetCO2 determined by régression analysis was maintained (R = 0.644, P < 0.001). Comparison of the individual and population correlation coefficients by Student’s t tests showed no significant difference, but a normal population distribution of the gradients (P < 0.05). None of the variables assessed could be determined to influence P(a-et)CO2 significantly. For many of the individual patients, however, the relationship between PaCO2 andetCO2 did not maintain a significant correlation throughout the study period. In the postoperative cardiac surgery patient population P(a-et)CO2 follows a normal distribution and PaCO2 andetCO2 maintain a statistically significant correlation. However, when evaluating individual patients, this relationship has wide variability.RésuméLes changements de gradient du CO2 arteriel et en fin d’expiration P(a-et)CO2 ont été étudiés en postop de chirurgie cardiaque chez les patients à partir du temps de l’admission aux soins intensifs, durant les changements du support cardiorespiratoire, jusqu’au temps de l’extubation endotrachéale. Les facteurs individuels évalués pour leurs effets sur la P(a-et)CO2 ont inclu la frequence de la ventilation mecanique, la perfusion d’agents vasoactifs (nitroglycérine, nitroprussiate, dopamine, dobutamine, et métariminol), et les changements pathophysiologiques hémodynamiques (index cardiaque, pression de l’artére pulmonaire, résistance indexée des vaisseaux pulmonaires, résistance indexée des vaisseaux systémiques, et la pression artérielle capillaire pulmonaire bloquee). Après acceptation par le Comité d’lnvestigation Clinique, 59 patients âgés de 63 ± 9 (41 à 75) ans, ont été étudiés et 382 gradients individuels ont été determinés. La P(a-et)CO2 moyenne était 5,47 ± 5,21 mmHg, avec une PaCO2 moyenne de 36,51 ± 5,89 mmHg et uneet CO2 moyenne de 31,04 ± 6,44 mmHg. Pour la population entière, la corrélation entre la PaCO2 et laet CO2 déterminee par analyse de régression était maintenue (R = 0,644, P < 0,001). Les comparaisons individuelles et les coefficients de correlation de la population étudiées par le Student’s t test n’ont pas montre de difference significative, mais une distribution normale de la population des gradients (P < 0,05). Aucune des variables etudiee n’a démontré un rôle significatif dans l’influence sur la P(a-et)CO2. Cependant pour plusieurs patients la relation entre la PaCO2 et laet CO2 n’a pas maintenue une correlation significative tout au long de I’etude. En période postopératoire de chirurgie cardiaque, la P(a-et)CO2 suit une courbe normale de distribution et la PaCO2 et laet CO2 ont maintenu une corrélation statistiquement significative. Cependant, quand on évalue les patients individuellement, cette relation présente une variabilité assez étendue.

The arterial to end-tidal carbon dioxide difference in neurosurgical patients during craniotomy

PETCO2 is often used as an estimate of PaCO2, with the understanding that PaCO2 usually exceeds PETCO2.During intraoperative craniotomies, because hyperventilation is used to therapeutically lower intracranial pressure, the difference between PaCO2 and PETCO2 (P(a-ET)CO2) has therapeutic implications. The P(a-ET)CO2 was hypothesized to be stable during craniotomies with relatively short-term monitoring and controlled cardiorespiratory variables. Thirty-five patients undergoing elective craniotomies were studied. Arterial blood gases (with PaCO2) were measured after induction of general anesthesia, after cranium opening prior to dural incision, and at start of closure; PETCO2 was simultaneously determined with infrared capnometry. The PaCO2 was 31.9 +/- 3.9 mm Hg (range, 24.8-46.7) (values are mean +/- SD) and PETCO2, 24.7 +/- 3.8 mm Hg (range, 16-34), with a P(a-ET)CO2 of 7.2 +/- 3.3 mm Hg (of 126 comparisons, range was -1.2-17.3). There was no correlation of P(a-ET)CO2 with blood pressure, heart rate, respiratory volumes, airway pressures, or inspired oxygen concentration. There was a significant positive correlation between PaCO2 and PETCO2 (r = 0.632, slope = 0.609) and P(a-ET)CO2 and PaCO2 (r = 0.46, slope = 0.391, P < 0.017, and r2= 0.22). Although changes in the study population of PaCO2 and PETCO2 correlated statistically (r = 0.818, slope = 0.76, P < 0.001, r (2)= 0.669), comparisons in 17 of 35 individuals werenotsignificant. On comparison of subsequent measurements, 18.4% of changes in PaCO2 and PETCO2 (although sometimes small) were in opposite directions. P(a-ET)CO2 did not change with time. The PETCO2 does not provide a stable reflection of PaCO2 in many patients undergoing craniotomies. (Anesth Analg 1995;81:806-10)

Hyperbaric nitrous oxide as a sole anesthetic agent in humans

Nitrous oxide (N2O) has been used to produce analgesia and anesthesia for more than 100 yr. However, because of its high MAC value (1.04), general anesthesia with N2O can usually be attained only in a hyperbaric environment. Because of the sparsity of documentation for human physiologic responses to hyperbaric N2O, we studied eight male volunteers at 2 ATA (1520 mm Hg) anesthetized with N2O only for periods of 2–4 h. N2O partial pressures ranged from 836 to 1368 mm Hg. The anesthetic state was associated with tachypnea, tachycardia, increases in systemic blood pressure, mydriasis, diaphoresis, and at times, clonus and opisthotonus. A stable level of physiologic activity was difficult to maintain.

Differences in Anesthetic Potency between Sprague-Dawley and Long-Evans Rats for Isoflurane but Not Nitrous Oxide

The mechanisms of action of halogenated (isoflurane) and inorganic (nitrous oxide (N2O)) anesthetic gases are postulated to differ. We tested the null hypothesis that there is no difference in anesthetic potency, as determined by MAC (the minimum alveolar anesthetic concentration preventing purposeful movement to supramaximal noxious stimulation in 50% of animals) between the Long-Evans (LE) and Sprague-Dawley (SD) rat strains for isoflurane and N2O. MAC values were determined using a 45-second standard supramaximal electrical stimulation. MAC of isoflurane for SD rats was 1.28 +/- 0.20 vol% (mean +/- standard deviation), but 0.98 +/- 0.14 vol% for LE rats (p = 0.001). MAC values for N2O were the same: 1.53 +/- 0.1 and 1.58 +/- 0.14 ata for SD and LE rats, respectively. The interstrain MAC difference for isoflurane, but not N2O, suggests different mechanisms of action for the two agents.

End-tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients.

The relationship between the arterial partial pressure of carbon dioxide (Paco2) and the end-tidal carbon dioxide partial pressure (PEtco2) was evaluated in 11 critically ill adult neurointensive care patients during mechanical ventilation. It was hypothesized that the Paco2 to PEtco2 gradient, or P(a-Et)co2, was maintained and that PEtco2 can be used to determine Paco2 accurately in these patients. After approval by the Clinical Investigations Committee, when clinically indicated arterial blood gases (with Paco2) were measured, the PEtco2 was determined from the capnograph (Hewlett Packard 78520A infrared capnometer). The P(a-Et)co2 was evaluated for possible effects from changes in the other monitored hemodynamic and respiratory parameters. Linear regression analysis was used to determine the significance of the relationship between Paco2 and PEtco2 and other assessed variables. Students t tests were used where applicable. A p value </=0.05 determined significance. One hundred thirty-five comparisons, 12.3 +/- 5.8 per patient, of Paco2 and PEtco2 were made. (All values are means +/- SD.) The P(a-Et)co2 was 6.9 +/- 4.4 mm Hg (-11-21 mm Hg), with Paco2 = 34 +/- 6 mm Hg and PEtco2 = 27 +/- 6 mm Hg. There was a significant correlation between Paco2 and PEtco2 values for the total study population (r = 0.72, p = 0.001). However, when the relationship between Paco2 and PEtco2 values for individual patients was analyzed, only seven of 11 patients (64%) had significant correlations. The direction of Paco2 change was inaccurately predicted by PEtco2 changes in 31.9% of measurements. PEtco2 does not provide a stable reflection of Paco2 in all neurointensive care patients. Arterial blood gases cannot be eliminated when monitoring respiratory acid-base balance in mechanically ventilated neurointensive care patients.

Direct Measurement of Nitrous Oxide Mac and Neurologic Monitoring in Rats During Anesthesia Under Hyperbaric Conditions

The minimum alveolar concentration (MAC) of nitrous oxide necessary to prevent purposeful movement in rats has not been directly measured;rather, it has been extrapolated because the required partial pressure exceeds 760 mm Hg, or 1 atm absolute pressure (ATA). Values reported have ranged from 1.36 to 2.20 ATA (136–220 vol%, or 1034–1672 mm Hg). By maintaining general anesthesia at 2.25 ATA (1710 mm Hg), we directly measured the nitrous oxide MAC in 17 Long-Evans rats during mechanical ventilation and monitoring of two-channel electroencephalogram, compressed spectral array and cortical evoked potentials, electrocardiograph, and respiratory and anesthetic gases by mass spectrometry. After a minimal stabilization period of 30 min during ventilation by 1.8 ATA nitrous oxide and 0.45 ATA oxygen, MAC measurements were begun. Each rat was given up to three noxious electrical stimulations of 50 V by 10-ms-duration pulses at 50/s for 45 s. The partial pressure of nitrous oxide was decreased by approximately 10% after each negative response. The MAC was taken as the nitrous oxide concentration midway between that at which there was no response and that at which the rat moved purposefully. The nitrous oxide MAC in Long-Evans rats was determined to be 1.55 ± 0.16 ATA (mean ± SD). Hyperbaric nitrous oxide decreased electroencephalogram wave frequency to a predominantly theta rhythm of increased amplitude. Cortical evoked potentials had decreased wave amplitudes and increased latencies with increasing partial pressures >0.75 ATA. General anesthesia with nitrous oxide at hyperbaric pressures allows direct measurement of the nitrous oxide MAC in rats and demonstrates neurophysiologic depressant effects on the electroencephalogram and somatosensory evoked potentials.

Preservation of Neurogenic Motor-Evoked Potentials During Isoflurane Electroencephalographic Burst Suppression in Rats

Study Design A prospective laboratory study was performed in a rat model. Objectives to test the hypothesis that neurogenic motor-evoked potentials are more resistant to suppressive changes from the volatile anesthetic isoflurane than cortically recorded somatosensory-evoked potentials and electroencephalography. Summary of Background Data Techniques for monitoring spinal cord motor tracts have been developed because sensory tract monitoring with somatosensory-evoked potentials is at times inadequate. Potentials from transcranial magnetic and electrical stimulation are very sensitive to anesthesia. Neurogenic motor-evoked potentials are thought to be more resistant. Methods Eight mature Sprague-Dawiey rats were studied during isoflurane general anesthesia. Two channel raw and computer-processed electroencephalograms, somatosensory-evoked potentials, and neurogenic motor-evoked potentials were recorded at six levels of anesthetic depths. Results Neurogenic motor-evoked potential amplitudes and latencies were unaltered. The electroenceph-alograms were depressed to isoelectricity with periodic burst activity above 1.27% isoflurane. Processed electroencephalograms showed depression above 0.72%. The somatosensory-evoked potentials were suppressed by increasing isoflurane and were not discernible at 2.2%. Conclusions Neurogenic motor-evoked potential signals are well preserved in rats during exposure to isoflurane concentrations that eliminate somatosensory-evoked potential waveforms and depress electroencephalograms to burst suppression.

Nonlinear additivity of nitrous oxide and isoflurane potencies in rats

PurposeTo test the hypothesis that the MAC values of nitrous oxide (N2O) and isoflurane were not linearly additive, as theorized by the postulated mode of action based on lipid solubility, in a rat model.MethodsEight Long Evans rats were randomly assigned to order of measurement of MAC for isoflurane and N2O alone and in combination using standard 45 sec supramaximal electrical stimulation (50 volts × 10 msec duration pulses at 50 · sec−1 applied for 45 sec sc to the lower abdominal groin area). The MAC of N2O was measured at hyperbaric compression to 2.25 atmospheres absolute, 1710 mmHg.ResultsThe MAC values found were: isoflurane − 0.98 ± 0.12 and N2O − 159 ± 12 volume (vol) %, or 1.59 ± 0.12 atmospheres absolute (ATA) (All values are mean ± standard deviation). The linear additivity theory suggests % MAC agent A + % MAC agent B = 1.0. However,% MAC isoflurane + % MAC N2O = 1.37 ± 0.15 (P < .001).ConclusionNonlinear additivity was demonstrated with direct MAC measurement for both isoflurane and N2O in rats. This suggests an agonist-antagonist relationship.RésuméObjectifÉvaluer l’hypothèse que les valeurs de CAM (concentration alvéolaire minimale) du protoxyde d’azote (N2O) et de l’isoflurane ne sont pas additives de façon linéaire, tel qu’envisagé à partir du mode d’action retenu, basé sur la solubilité lipidique, et ce chez le rat comme modèle.MéthodesHuit rats de souche Long Evans ont été attribués de façon aléatoire à la séquence de mesure de la CAM pour l’isoflurane et le N2O de façon isolée ainsi que pour la combinaison des deux. Le test utilisé a été une stimulation électrique supra maximale standard d’une durée de 45 sec (stimuli de 50 volts, d’une durée de 10 msec, d’une fréquence de 50 · sec−1 appliqués durant 45 sec par voie sc à la région inguinale basse). La CAM du N2O a été mesurée en condition hyperbare à 2.25 atmosphères, soit 1710 mmHg.RésultatsLes CAM trouvées étaient les suivantes: isoflurane: 0.98 ± 0.12 et N2O: 159 ± 12 vol % ou 1.59 0.12 atmosphères en valeur absolue (ATA) (toutes les valeurs représentent la moyenne ± écart type). La théorie de l’addition linéaire propose que% CAM agent A +% CAM agent B = 1. Cependant, dans cette étude, le % CAM isoflurane +% CAM N2O = 1.37 ± 0.15 (P < 0,001).ConclusionUne additivité non linéaire a été démontrée par des mesures directes de la CAM de l’isoflurane et du N2O chez le rat. Ceci suggère une relation agoniste-antagoniste.

Detection of venous air embolism in dogs by emission spectrometry

Emission spectrometers provide alternative, relatively inexpensive methods for detecting the concentration of respiratory gas nitrogen. Mass spectrometers are accepted as reliable monitors of end-tidal nitrogen for detection of venous air embolisms. We evaluated an inexpensive emission spectrometer for detecting changes in nitrogen levels and compared it with a mass spectrometer for detecting increased endtidal nitrogen levels in dogs with venous air embolisms. During in vitro gas flow studies (helium; oxygen; helium/ oxygen mixtures; or 70% nitrous oxide/30% oxygen with 0, 1, 2, or 3% isoflurane), air boluses (0.01 to 5.0 ml) were injected into a gas flow circuit and outlet nitrogen levels were measured by a Collins 21232 emission spectrometer. Responses were greater after each bolus when helium rather than oxygen was the major diluent gas. During in vivo studies, 5 dogs were anesthetized, ventilated, denitrogenated, and given venous air embolisms (0.1, 0.5, and 1.0 ml. kg-1) during oxygen and then during Heliox (20% oxygen:80% helium) breathing. End-tidal nitrogen increased approximately two-fold after venous air embolisms given during Heliox as compared with oxygen ventilation. In all 0.1-ml. kg-1 venous air embolisms end-tidal nitrogen increased when the emission spectrometer was used, but venous air embolisms less than 1.0 ml. kg-1 were not consistently detected by mass spectrometry. Emission spectrometry can be used to detect increased end-tidal nitrogen levels indicative of venous air embolism and may be a more sensitive detector than mass spectrometry. Its sensitivity and relatively low cost (one-eighth of a magnetic fixed-sector mass spectrometer) make it a great potential monitor for both clinical detection of venous air embolism and air embolism research.