Search

We have employed a genetic approach to study the resistance of tomato to the phytopathogenic bacterium Pseudomonas syringae pv tomato. Resistance to P. s. tomato depends upon expression of the Pto locus in tomato, which encodes a protein with similarity to serine/threonine protein kinases and recognizes pathogen strains expressing the avirulence gene avrPto. Eleven tomato mutants were isolated with altered resistance to P. s. tomato strains expressing avrPto. We identified mutations both in the Pto resistance locus and in a new locus designated Prf (for Pseudomonas resistance and fenthion sensitivity). The genetic approach allowed us to dissect the roles of these loci in signal transduction in response to pathogen attack. Lines carrying mutations in the Pto locus vary 200-fold in the degree to which they are susceptible to P. s. tomato strains expressing avrPto. The pto mutants retain sensitivity to the organophosphate insecticide fenthion; this trait segregates with Pto in genetic crosses. This result suggested that contrary to previous hypotheses, the Pto locus controls pathogen recognition but not fenthion sensitivity. Interestingly, mutations in the prf locus result in both complete susceptibility to P. s. tomato and insensitivity to fenthion, suggesting that Prf plays a role in tomato signaling in response to both pathogen elicitors and fenthion. Because pto and prf mutations do not alter recognition of Xanthomonas campestris strains expressing avrBsP, an avirulence gene recognized by all tested tomato cultivars, Prf does not play a general role in disease resistance but possibly functions specifically in resistance against P. s. tomato. Genetic analysis of F2 populations from crosses of pto and prf homozygotes indicated that the Pto and Prf loci are tightly linked.

Objective: We wished to determine whether the individual bias (mean difference) and precision (standard deviation of the difference) values of 2 variables, arterial oxygen saturation (SaO2) and mixed venous oxygen saturation (SvO2), could be used to predict the bias and precision values of the combined dual oximetry variable (SaO2-SvO2)., Methods: We simultaneously measured SaO2 by pulse oximetry and arterial blood gas co-oximetry and SvO2 by fiberoptic reflectance oximetry pulmonary artery catheter and venous blood gas co-oximetry in 238 data sets from 55 patients. Three different methods were used to predict the standard deviation of the difference of (SaO2-SvO2) [s delta(SaO2-SvO2)]: simple sum, root mean square (RMS) error, and RMS error with correction term. We derived the equation for the RMS error with correction term because initial results showed that the simple sum and RMS error methods did not predict s delta(SaO2-SvO2) well. The correction term accounts for the non-independence of simultaneous SaO2 and SvO2 measurements., Results: The observed overall bias of the SaO2, SvO2, and (SaO2-SvO2) measurement methods were 0.17, -1.76, and 1.94, respectively. The observed overall s delta(SaO2-SvO2) of the (SaO2-SvO2) measurement method was 5.12. The simple sum method overestimated the actual s delta(SaO2-SvO2) by 38%, the RMS error method differed from the actual s delta(SaO2-SvO2) by 3%, and the RMS error with correction term method matched the actual s delta(SaO2-SvO2)., Conclusion: The bias of a (SaO2-SvO2) measurement method is simply the bias of the SaO2 measurement method less the bias of the SvO2 measurement method. s delta(SaO2-SvO2) is best predicted by the derived equation, RMS error with correction term. The same principles and equations also apply to other situations in which 2 variables with the same dimensions are combined into 1 variable, such as (PaCO2-EtCO2) gradients and perfusion-pressure gradients. Although the difference between the s delta(SaO2-SvO2) predicted by the RMS error equation and the derived RMS error equation with correction term was small, the difference may be significant for other combined variables.

Background: Previous studies have shown that pulse oximeters whose sensors are positioned improperly may yield erroneously low saturation (SpO2) values on normoxemic subjects. The behavior of oximeters with malpositioned sensors during hypoxemia has not been studied. The current study is aimed at determining the behavior of several different pulse oximeters over a wide range of arterial oxygen saturation (SaO2)., Methods: In each of 12 healthy volunteers, a radial artery cannula was inserted, and eight different pulse oximeters, five of which had malpositioned sensors, were applied. Subjects breathed controlled mixtures of nitrogen and oxygen to slowly vary their SaO2 from 100% to 70%. Arterial blood samples were analyzed and pulse oximeter data were recorded at five stable SaO2 values for each subject., Results: The oximeters with malpositioned sensors vary greatly in their behavior, depending on both the actual SaO2 and the manufacturer and model. One oximeter underestimated saturation at all SaO2 values, while three others underestimated at high SaO2 and overestimated at low SaO2. Linear regression analysis shows a decrease in the slope of SpO2 versus SaO2 in most cases, indicating a loss of sensitivity to SaO2 changes. Between-subject variation in response curves was significant., Conclusions: The calibration curves of the pulse oximeters studied were changed greatly by sensor malpositioning. At low SaO2 values, these changes could cause the oximeter to indicate that a patient was only mildly hypoxemic when, in fact, hypoxemia was profound. It is recommended that sensor position be checked frequently and that inaccessible sensor locations be avoided whenever possible.

Anaesthetic residents used bag valve mask (BVM) or mouth mask (MM) ventilation, both with an O2 flow of 15 l min-1 to ventilate 30 ASA I or II anaesthetised patients for 4 min prior to endotracheal intubation. Mean nasopharyngeal O2 was higher with BVM (BVM 95% (S.D. 3%) MM 54% (S.D. 12%)). End tidal CO2 (ETCO2) was similar in both groups (ETCO2% at 4 min: BVM 4.65 (S.D. 0.84) MM 4.53 (S.D. 0.54)) but respiratory rate was faster with BVM (BVM 17 min-1 (S.D. 5) MM 12 min-1 (S.D. 4)). Peak (Paw) and mean (Paw) airway pressures were higher with MM and MM produced significant expiratory pressure [cmH2O: BVM Paw 16.7 (S.D. 5.3) Paw 4.2 (S.D. 2.1) MM: Paw 20.9 (S.D. 5.2) Paw 7.8 (S.D. 2.1)) minimum expiratory pressure: MM 2.4 (S.D. 1.1) BVM 0.2 (S.D. 0.4). Gastric insufflation was detected in two MM and two BVM patients. This tended to be more severe with MM ventilation. Although MM ventilation has some important disadvantages it can be used effectively by resuscitators with little or no experience in its use.

Background: We describe the anesthetic management for a new surgical procedure: laser ablation of emphysematous bullae via thoracoscope. Although thoracoscopy is not new, this is the first description of a series of patients with bilateral, chronic lung disease who underwent long periods of one-lung ventilation (OLV) during thoracoscopic therapy., Methods: Twenty-six laser ablation procedures were performed in 22 patients. The patients were elderly (mean age 63 yr) with a large incidence of coexisting cardiovascular disease. Most required chronic home oxygen therapy. Patients were monitored invasively, and hemodynamic data were recorded every 5 min. Arterial blood gas analyses were performed every 15 min. Comparisons were made between three intraoperative periods: two-lung ventilation (TLV) before thoracoscopy, OLV during thoracoscopy, and TLV after thoracoscopy., Results: All patients survived the operation despite a mean OLV duration of 170 min, but several experienced serious intraoperative problems, such as hypoxemia or hypotension. Hypoxemia was treated with nondependent lung continuous positive airway pressure and dependent lung positive end-expiratory pressure. In all patients the lungs were adequately ventilated, but bronchopleural fistulae occurred upon return to TLV in every case. The resulting air leaks, often 50% of inspired tidal volume, required the use of a pressure-cycled ventilator to maintain oxygenation. Postoperative air leaks greater than 50% of inspired tidal volume usually required subsequent surgical correction, while smaller leaks resolved spontaneously. Mechanical ventilation was required for an average of 5 days. Eighty-four percent have survived at least 6 months, and nearly all survivors report symptomatic improvement., Conclusions: Ablation of bullae appears to provide symptomatic improvement, and thoracoscopy might be better tolerated than thoracotomy, especially in patients with severe bullous emphysema.

To determine the effect of increasing supplementary oxygen flow during ventilation with the Laerdal pocket mask 24 subjects ventilated a modified recording mannikin for four 90 s periods using the mask with oxygen flows of 5 l, 10 l, 15 l and 20 l.min-1. Oxygen concentration increased and carbon dioxide concentration decreased with increasing oxygen flow. Tidal volume also increased with oxygen flow. The delivered oxygen concentrations were lower than previously reported at all four rates; however, mask function improved with increasing flow up to 20 l.

Transcutaneous oxygen tension (PtcO2) is often used to monitor neonates and infants in special care units and the operating room. The transcutaneous index (TCI = PtcO2/arterial oxygen tension [PaO2]) is known to depend both on age and on cardiac index but is assumed to be independent of other physiologic variables. In this study we have shown that TCI also depends upon arterial carbon dioxide tension (PaCO2). Five young pigs were anesthetized and paralyzed and their lungs mechanically ventilated while they were monitored with PtcO2 electrodes and serial arterial blood gas analyses. For a 45 degrees C PtcO2 sensor, the mean TCI during normocapnia was 0.78, whereas during hyperventilation (PaCO2 = 20 mmHg) the mean TCI was reduced 65%, to 0.27. The corresponding TCI values for a 43 degrees C sensor were 0.33 and 0.065, representing an 80% decrease in TCI during hyperventilation. Hypoventilation had little effect upon TCI as long as hypoxemia was avoided. Twelve awake adult volunteers with radial artery cannulas were monitored with PtcO2 sensors at several body sites and two sensor temperatures. For a 44 degrees C sensor on the chest, the mean TCI decreased from 0.77 at normocapnia to 0.60 at a PaCO2 of 17 mmHg, a 22% change. For the same sensor on the foot, TCI decreased from 0.63 to 0.32, a 49% change. For a 42 degrees C sensor under the same conditions, the corresponding TCI decreases were 51 and 64%. Six of the volunteers were also monitored with laser-Doppler skin blood flow probes located on the chest, hand, and foot.(ABSTRACT TRUNCATED AT 250 WORDS)

The accuracy of pulse oximetry (for pulse hemoglobin oxygen saturation [SpO2]) and mixed venous oximetry (for mixed venous hemoglobin oxygen saturation [SvO2]) was assessed during progressive normovolemic anemia in dogs. Splenectomized mongrel dogs under general anesthesia were monitored with a three-wavelength pulmonary artery oximeter catheter (10 dogs) and a pulse oximeter (11 dogs). Data were collected while fractional inspired oxygen concentration (FIO2) was varied from 1.00 to 0.05 in seven steps. The dogs then underwent isovolemic hemodilution, and the FIO2 was again varied. This sequence continued until data no longer could be obtained. The accuracy of each device was assessed by determining the bias (the average difference between the continuous monitor oximeter and the bench oximeter) and the precision (the standard deviation of the difference). For the three-wavelength Oximetrix catheter (for hemoglobin oxygen saturation denoted here SoxO2), the overall bias (SoxO2 - SvO2) and precision were -0.7 +/- 8.6% for the 193 data points. The accuracy as assessed by bias and precision for SoxO2 was similar for hematocrits of 40-15%. (Bias +/- precision was 2.1 +/- 5.7% for hematocrits greater than 40%, and -1.1 +/- 7.5% for hematocrits of 15% to 19%). At hematocrits between 10 and 14%, the precision worsened to 12%, and for hematocrits less than 10% the bias +/- precision was -11.5 +/- 11.8%. The overall SpO2 accuracy was 0.2 +/- 7.6% for 178 points. The pulse oximeter's accuracy was similar, down to hematocrits of 10%. Below 10%, the bias and precision worsened to -5.4 +/- 18.8%.(ABSTRACT TRUNCATED AT 250 WORDS)

Miniaturized sensors based upon the principles of optical fluorescence can measure the pH, PCO2, and PO2 of liquid or gas media. A prototype of a three-component fiberoptic sensor has been developed for intraarterial application by CDI, 3M Health Care, Irvine, California. We report the first study of this continuous intraarterial monitor in patients undergoing surgical procedures under general anesthesia. Fourteen patients participated in the study. The fiberoptic sensor was calibrated before insertion and then passed through an existing 18-gauge radial artery cannula. Blood samples were drawn at frequent intervals through the same cannula for in vitro blood gas analysis. For each of the 87 arterial blood gas samples obtained, the in vitro values of pHa, PaCO2, and PaO2 were compared with simultaneous readings from the fiberoptic sensor. For pHa, the mean error (error = fiberoptic value minus in vitro value) or "bias" of the fiberoptic data was -0.032 and the standard deviation of error or "precision" was 0.042. For PaCO2, the bias was -3.8 mm Hg and the precision was 4.7 mm Hg. For PaO2, the bias was -9.0 mm Hg and the precision was 23.3 mm Hg. For PaO2 values less than 175 mm Hg, the bias was -8.5 mm Hg and the precision was 8.3 mm Hg. Expressed in terms of percentage errors, the bias +/- precision values were -11.5% +/- 13.3% for PaCO2, and -6.2% +/- 10.0% for PaO2. The duration of the surgical procedures ranged from 1.6 to 8 h with an average of 4.2 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Among the sequence of events which occur during photodynamic therapy (PDT) are depletion of oxygen and disruption of tumor blood flow. In order to more clearly understand these phenomena we have utilized transcutaneous oxygen electrodes to monitor tissue oxygen disappearance. These results provide, for the first time, non-invasive real-time information regarding the influence of light dose on tissue oxygenation during irradiation. Measurements were conducted on transplanted VX-2 skin carcinomas grown in the ears of New Zealand white rabbits. Rabbits were treated with Photofrin II and tumors were irradiated with up to 200 kJ/m2 (500 W/m2) of 630-nm light. Substantial reductions in tumor oxygen tension were observed upon administration of as little as 20 kJ/m2. For a series of brief irradiations, oxygen tension was modulated by the appearance of laser light. Tissue oxygen reversibility appeared to be dependent upon PDT dose. Long-term, irreversible tissue hypoxia was recorded in tumors for large (200 kJ/m2) fluences. These results suggest that transcutaneous oxygen tension may be useful as a general indicator of the effectiveness of PDT and as an in situ predictor of the energy required to elicit tumor damage.

In a recent study, we compared a new intraarterial fiberoptic "optode" probe to continuously measure arterial oxygen and carbon dioxide tensions and pH with intermittently drawn blood samples in patients undergoing surgery. In one patient with a diagnosis of Arnold-Chiari type I malformation with outflow obstruction of the fourth ventricle, a major pulmonary air embolism occurred while the patient was undergoing suboccipital craniectomy and cervical laminectomy in the prone position. Three hours after the incision the optode-displayed oxygen tension decreased from a stable value of 225 +/- 8 mm Hg to 63 mm Hg over a 10-minute period. During the same interval, carbon dioxide tension increased and end-tidal carbon dioxide decreased; shortly thereafter, transcutaneous oxygen tension decreased also. Within 20 minutes after the inspired gas mixture was changed to 100% oxygen, the patient's respiratory variables returned to near baseline. No further complications ensued. This is the first time continuously monitored arterial oxygen tension values during a pulmonary embolism have been reported. With further refinement, intraarterial optode probes will add another valuable method of detecting pulmonary air embolism.

We transformed tobacco plants with a soybean beta-conglycinin gene that encodes the 1.7-kilobase beta-subunit mRNA. We showed that the beta-conglycinin mRNA accumulates and decays during tobacco seed development and that beta-conglycinin mRNA is undetectable in the tobacco leaf. We utilized in situ hybridization to localize beta-conglycinin mRNA within the tobacco seed. beta-Conglycinin mRNA is not detectable within the endosperm but is localized within specific embryonic cell types. The highest concentration of beta-conglycinin mRNA is found in cotyledon storage parenchyma cells. We conclude that sequences required for embryo expression, temporal control, and cell specificity are linked to the beta-conglycinin gene, and that factors regulating beta-conglycinin gene expression are compartmentalized within analogous soybean and tobacco seed regions.

The pulse oximeter estimates arterial hemoglobin saturation by measuring the light absorbance of pulsating vascular tissue at two wavelengths. The relationship between measured light absorbances and saturation was developed empirically and is built into the oximeter software. Studies in human volunteers have shown good performance of the device in healthy adults for saturations in the range of 70 to 100%. Studies in the operating room and intensive care unit have established its clinical accuracy and usefulness. The pulse oximeter has already found a number of clinical applications outside of the operating room, such as monitoring during patient transport, respiratory monitoring during narcotic administration, and evaluation of home-oxygen therapy. To use this monitor to its full potential, we must be aware of its limitations as well as its advantages. Because of the nature of the HbO2 dissociation curve, saturation measurements will not be sensitive to changes in PaO2 when the PaO2 is greater than 100 torr. This also implies that the pulse oximeter may fail to detect an inadvertent endobronchial intubation in the operating room. It may take minutes to detect an esophageal intubation in a well-preoxygenated patient. When desaturation does occur, the pulse oximeter detects it quickly, accurately, and reliably. Since the pulse oximeter uses two wavelengths of light, it cannot distinguish more than two hemoglobin species. Thus, COHb and MetHb will cause errors in SpO2 if present in large amounts. Intravenously administered dyes can also cause errors because of their absorbance properties, particularly methylene blue and indocyanine green. The pulse oximeter may be unable to detect an adequate signal during abnormal hemodynamic conditions. The pulse oximeter is one of the most important advances in noninvasive monitoring because it provides a means of continuously and quickly assessing arterial blood oxygenation. It is easy to use and interpret, requires little setup time, and poses no additional risks to the patient. Pulse oximetry may soon be a standard of practice for routine monitoring in any clinical setting in which the patient is at risk of hypoxemia.

A new device has been developed to estimate continuously and noninvasively cardiac output from the thoracic electrical bioimpedance (CObi). CObi was compared to cardiac output by thermodilution (COtd) in five anesthetized dogs. Blood pressure, blood volume, and blood flow were manipulated by hemorrhage and infusions of sodium nitroprusside and phenylephrine. These data were used to determine the correlation between CObi and COtd under conditions of hypotensive normal flow and normotensive low flow, as well as during hemorrhagic shock and resuscitation. The CObi device was calibrated in vivo to COtd for each dog at the beginning of each experiment. CObi had a significant positive correlation with COtd throughout the experiments (r = 0.84, slope = 0.91, intercept = 0.55, p less than 0.01), and CObi predicted COtd with a standard error of the estimate of 0.81 L/min. Neither heart rate nor mean arterial pressure was significantly correlated with COtd or CObi. During severe hemorrhagic shock, CObi could not determine cardiac output in two of the dogs when COtd averaged 1.7 L/min. These data indicate that CObi is a blood-flow related variable that can be monitored continuously.

Transcutaneous PO2 sensors have been developed over the past ten years from the same basic electrodes used in conventional blood-gas machines. The skin is heated to enable the skin surface sensors to respond quickly to the gas tensions beneath them. PtcO2 is a variable that reflects the PO2 in the peripheral tissue. PtcO2 has its own range of normal values, and it responds to cardiopulmonary changes that affect tissue oxygenation. In most patients, those without decreased cardiac output, PtcO2 follows the trend of PaO2 and decreases relative to PaO2 with increasing patient age (see Table 2). In the presence of severely reduced cardiac output and peripheral perfusion, the PtcO2 values will deviate from their relationship with the arterial tensions and become blood flow dependent, thus providing quantitative information regarding blood flow. The technique of PtcO2 monitoring likely will gain wider acceptance because it is a noninvasive and continuous monitor that provides useful information regarding tissue oxygenation.

We investigated the chromosomal organization and developmental regulation of soybean beta-conglycinin genes. The beta-conglycinin gene family contains at least 15 members divided into two major groups encoding 2.5-kilobase and 1.7-kilobase embryo mRNAs. beta-Conglycinin genes are clustered in several DNA regions and are highly homologous along their entire lengths. The two groups differ by the presence or absence of specific DNA segments. These DNA segments account for the size differences in beta-conglycinin mRNAs. The 2.5-kilobase and 1.7-kilobase beta-conglycinin mRNAs accumulate and decay at different times during embryogenesis. By contrast, genes encoding these mRNAs are transcriptionally activated and repressed at the same time periods. Our studies indicate that the beta-conglycinin family evolved by both duplication and insertion/deletion events, and that beta-conglycinin gene expression is regulated at both the transcriptional and posttranscriptional levels.

This study compares two noninvasive techniques for monitoring the partial pressure of carbon dioxide (PCO2) in 24 anesthetized adult patients. End-tidal PCO2 (PetCO2) and transcutaneous PCO2 (PtcCO2) were simultaneously monitored and compared with arterial PCO2 (PaCO2) determined by intermittent analysis of arterial blood samples. PETCO2 and PtcCO2 values were compared with PaCO2 values corrected to patient body temperature (PaCO2T) and PaCO2 values determined at a temperature of 37 degrees C (PaCO2). Linear regression was performed along with calculations of the correlation coefficient (r), bias, and precision of the four paired variables: PETCO2 versus PaCO2 and PaCO2T (n = 211), and PtcCO2 versus PaCO2 and PaCO2T (n = 233). Bias is defined as the mean difference between paired values, whereas precision is the standard deviation of the difference. The following values were found for r, bias, and +/- precision, respectively. PETCO2 versus PaCO2: 0.67, -7.8 mm Hg, +/- 6.1 mm Hg; PETCO2 versus PaCO2T: 0.73, -5.8 mm Hg, +/- 5.9 mm Hg; PtcCO2 versus PaCO2: 0.87, -1.6 mm Hg, +/- 4.3 mm Hg; PtcCO2 versus PaCO2T: 0.84, +0.7 mm Hg, +/- 4.8 mm Hg. Although each of these PCO2 variables is physiologically different, there is a significant correlation (P less than 0.001) between the noninvasively monitored values and the blood gas values. Temperature correction of the arterial values (PaCO2T) slightly improved the correlation, with respect to PETCO2, but it had the opposite effect for PtcCO2. In this study, the chief distinction between these two noninvasive monitors was that PETCO2 had a large negative bias, whereas PtcCO2 had a small bias. We conclude from these data that PtcCO2 may be used to estimate PaCO2 with an accuracy similar to that of PETCO2 in anesthetized patients.

Both halothane and nitrous oxide can be reduced at the cathode of a polarographic oxygen electrode, causing the electrode current to drift upward and report falsely high oxygen tension. Because transcutaneous oxygen tension is measured by a heated oxygen electrode, there is a potential for significant upward drift of these values. To examine the clinical significance of this drift, the following study was performed. Transcutaneous oxygen tension sensors were calibrated at oxygen tensions of 0 mm Hg and 157 mm Hg (room air) just before clinical use during anesthesia. This calibration was rechecked immediately upon removal of the sensor from the patient at the end of the anesthesia. The predominant anesthetic agent used and the duration of monitoring were noted from the record. Data were collected from 208 patients representing a total of 463.6 hours of anesthesia. The patients were divided into five groups based on anesthetic administered: halothane, enflurane, isoflurane, nitrous oxide-narcotic, and local/regional. The mean zero point recalibration value was 0.4 mm Hg or less for all agents except halothane, for which it was 1.8 +/- 3.2 mm Hg. This halothane drift was significantly greater than that for the other agents (P less than 0.01). Room air recalibration was not significantly different in any of the five groups, varying from 160 +/- 4.9 mm Hg for halothane to 157 +/- 4.9 mm Hg for enflurane. All these drift values are within the manufacturer's specifications. We conclude that the drift of the transcutaneous oxygen tension sensor due to anesthetic agents is not clinically significant. However, caution should be exercised when halothane is used during an extremely long period of anesthesia.

The performance of three commercially available pulse oximeters was assessed in five anesthetized dogs in which increasing levels of methemoglobin were induced. Hemoglobin oxygen saturation in each dog was monitored with three pulse oximeters (Nellcor N-100, Ohmeda 3700, and Novametrix 500) and a mixed venous saturation pulmonary artery catheter (Oximetrix Opticath). Arterial and mixed venous blood specimens were analyzed for PaO2, PaCO2, and pHa using standard electrodes. An IL-282 Co-oximeter was used on the same specimens to determine oxyhemoglobin and methemoglobin as percentages of total hemoglobin. Methemoglobin levels of up to 60% were induced by intratracheal benzocaine. As MetHb gradually increased while the dogs were breathing 100% inspired oxygen, the pulse oximeter saturation (SpO2) overestimated the fractional oxygen saturation (SaO2) by an amount proportional to the concentration of methemoglobin until the latter reached approximately 35%. At this level the SpO2 values reached a plateau of 84-86% and did not decrease further. When, at fixed methemoglobin levels, additional hemoglobin desaturation was induced by reducing inspired oxygen fraction, SpO2 changed by much less than did SaO2 (regression slopes from 0.16 to 0.32). Thus, at high methemoglobin levels SpO2 tends to overestimate SaO2 by larger amounts at low hemoglobin saturations. Plots of SpO2 versus functional saturation (oxyhemoglobin/reduced hemoglobin plus oxyhemoglobin) show an improved but still poor relationship (regression slopes from 0.32 to 0.46). The Oximetrix Opticath pulmonary artery catheter behaves similarly but provides somewhat better agreement with functional saturation than do the pulse oximeters in the presence of methemoglobinemia. Pulse oximetry data (SpO2) should be used with caution in patients with methemoglobinemia.

An experimental study using a new fiberoptic sensor for the continuous intraarterial measurement of oxygen tension is described. This "optode" sensor uses the phenomenon of fluorescence quenching to determine the oxygen tension of the surrounding medium. To assess the accuracy of this device, we anesthetized 4 dogs and monitored them continuously with arterial catheters and an intraarterial optode probe, and intermittently with arterial blood gas analysis. The inspired oxygen fraction was varied from 1.0 to 0.1, and arterial blood gases were measured for comparison with the optode reading. Two hundred ninety data sets yielded a correlation coefficient of 0.96, with a linear regression slope of 0.98 and intercept of 5.1 mm Hg. In the 72 data sets from the last dog, the bias and precision of the optode arterial oxygen tension values were -10.3 mm Hg and 20.0 mm Hg, respectively. The optode probe was easily inserted through a 20-gauge catheter and did not interfere with continuous arterial pressure measurement or blood sampling. This study suggests that the optode has great potential as a continuous, real-time monitor of arterial oxygen tension.

Transcutaneous PO2 (PtcO2) and liver surface PO2 (PIO2) were measured in six mongrel dogs during hemorrhagic shock, normotensive shock, and volume resuscitation. Normotension was produced during extreme hypovolemia by an infusion of phenylephrine. PtcO2 and PlO2 were compared to each other and to hemodynamic and oxygen transport variables. PtcO2 and PlO2 correlated well with cardiac index (CI) r = .71 and .86, respectively; n = 60) and with each other (r = .79; n = 60). Heart rate, mean arterial pressure (MAP), and PaO2) correlated less with PtcO2 or PlO2. During the normotensive shock period, PtcO2, PIO2, CI, oxygen delivery (DO2), and oxygen consumption (VO2) were all severely decreased, while PaO2 and MAP were normal and lactic acid concentrations were elevated. It was concluded that PtcO2 follows changes in PlO2 during hypotensive and normotensive low cardiac output shock in mongrel dogs. Low PtcO2 values are associated with low values of PlO2, DO2, VO2, and rising lactic acid concentrations in dogs. These animal data imply that low PtcO2 values encountered in clinical monitoring during anesthesia and surgery may correspond to decreased blood volume, blood flow, and PlO2.

Anesthesia and surgery have a wide range of effects on the cardiovascular system. Even in healthy patients having minor operations, anesthetic agents can cause significant cardiac depression and hemodynamic instability. Virtually all anesthetic agents have intrinsic myocardial depressant properties, although some may mask this with sympathetic stimulation. The vasodilatory effects of the volatile agents can result in serious hypotension when combined with this negative inotropy. In the patient with pre-existing cardiac disease, these cardiovascular anesthetic effects become much more serious. These patients will not tolerate wide swings of hemodynamic variables, and the cardiodepressant effects of anesthetics are more pronounced in them. The stress of anesthesia and surgery frequently unmasks previously undiagnosed heart disease. Surgery itself provides many insults to the cardiovascular system, and these may be additive with the effects of anesthesia. These include loss of blood and other volume shifts, release of various substances into the circulation, hypothermia, sudden changes in cardiac preload and afterload, myocardial ischemia, and effects of drugs or blood products given for surgical reasons. The signs and symptoms of these surgical stresses to the cardiovascular system are often masked by anesthesia.

Rapid and reliable detection of inadvertent endobronchial intubation is an essential function of oxygen monitoring. We have studied the detection of this event by using three oxygen monitoring techniques: pulse oximetry, transcutaneous measurement of oxygen tension, and intraarterial fiberoptic measurement of oxygen tension. Four dogs were anesthetized, intubated, and monitored with these three techniques and with arterial and central venous cannulas. Endotracheal tubes were moved from the trachea into the right mainstem bronchi at several inspired oxygen fraction (FIO2) values for each dog, and the responses of the oxygen monitors were recorded for 20 minutes thereafter. The pulse oximeter showed little change in oxygen saturation (SpO2) during endobronchial intubation at FIO2 values above 0.3. SpO2 decreased by an average of 1.3 +/- 2.1% at an FIO2 of 1.0 and by 4.0 +/- 4.1% at an FIO2 of 0.5. Simultaneously measured transcutaneous oxygen tensions decreased by 42 to 64% and the optode reading decreased by 64 to 79%. At lower FIO2 values, the changes in SpO2 were more significant: a decrease of 6.0 +/- 6.3% at an FIO2 of 0.3 and of 9.8 +/- 6.1% at an FIO2 of 0.2. The transcutaneous oxygen and optode readings decreased by 31 to 45% under these conditions. Endobronchial intubations at FIO2 values greater than 0.3 may not yield immediate decreases in arterial saturation and hence may go undetected by pulse oximetry. Transcutaneous oxygen tension decreases significantly with endobronchial intubation at any FIO2. The experimental, intraarterial optode consistently yielded the greatest changes with the fastest time response.

Five dogs were anesthetized, intubated, and ventilated with various mixtures of oxygen, nitrogen, and carbon monoxide. Each dog was monitored with arterial and pulmonary artery catheters, a transcutaneous PO2 analyzer, and two pulse oximeters. An IL-282 Co-oximeter was used to periodically measure arterial oxyhemoglobin (O2Hb) and carboxyhemoglobin (COHb) as percentages of the total hemoglobin. The PaO2, PaCO2, and pHa were measured in the same blood specimens using standard electrodes. When the inspired oxygen concentration was reduced in the absence of COHb, the pulse oximeter saturation (SpO2) estimated O2Hb with reasonable accuracy. COHb levels were then varied slowly from 0-75% in each dog. As the COHb level increased and oxyhemoglobin decreased, both pulse oximeters continued to read an oxygen saturation of greater than 90%, while the actual O2Hb fell below 30%. In the presence of COHb, the SpO2 is approximately the sum of COHb and O2Hb, and, thus, may seriously overestimate O2Hb. The pulse oximeter, as the sole indicator of blood oxygenation, should, therefore, be used with caution in patients with recent carbon monoxide exposure. On the other hand, transcutaneous PO2 falls linearly as COHb increases, and reaches about one-fifth of its initial value at the highest COHb levels despite the maintenance of constant arterial PO2.