Oxygenator exhaust capnography as an index of arterial carbon dioxide tension during cardiopulmonary bypass using a membrane oxygenator

We have studied the relationship between the partial pressure of carbon dioxide in oxygenator exhaust gas (PECO2) and arterial carbon dioxide tension (PaCO2) during hypothermic cardiopulmonary bypass with non- pulsatile flow and a membrane oxygenator. A total of 172 paired measurements were made in 32 patients, 5 min after starting cardiopulmonary bypass and then at 15-min intervals. Additional measurements were made at 34 degrees C during rewarming. The degree of agreement between paired measurements (PaCO2 and PECO2) at each time was calculated. Mean difference (d) was 0.9 kPa (SD 0.99 kPa). Results were analysed further during stable hypothermia (n = 30, d = 1.88, SD = 0.69), rewarming at 34 degrees C (n = 22, d = 0, SD = 0.84), rewarming at normothermia (n = 48, d = 0.15, SD = 0.69) and with (n = 78, d = 0.62, SD = 0.99) or without (n = 91, d = 1.07, SD = 0.9) carbon dioxide being added to the oxygenator gas. The difference between the two measurements varied in relation to nasopharyngeal temperature if PaCO2 was not corrected for temperature (r2 = 0.343, P = < 0.001). However, if PaCO2 was corrected for temperature, the difference between PaCO2 and PECO2 was not related to temperature, and there was no relationship with either pump blood flow or oxygenator gas flow. We found that measurement of carbon dioxide partial pressure in exhaust gases from a membrane oxygenator during cardiopulmonary bypass was not a useful method for estimating PaCO2.      

Alpha-stat capnography for the Sorin Monolyth oxygenator

Monitoring the carbon dioxide exhaust of an oxygenator is an inexpensive method to accurately predict and control the arterial carbon dioxide tension during cardiopulmonary bypass (CPB). The partial pressure of carbon dioxide in the exhaust ventilating gas (p exCO 2) was continuously monitored from the capnograph port of the Sorin Monolyth oxygenator during CPB. At the time of routine arterial blood gas sampling, the arterial blood temperature (ABT) was recorded along with the p exCO 2 from the capnograph monitor. The arterial carbon dioxide tension (paCO 2) from the arterial blood sample analysis was then statistically analyzed and related to the p exCO 2 and ABT. The statistical relationship of p exCO 2 and ABT while employing alpha stat ventilation resulted in an exponential regression with a correlation coefficient of 0.98. The exponential regression is unique to each manufacturer's oxygenator; we have titled this the "regression signature." This regression signature can be easily learned and employed by the perfusionist during CPB as an aid in controlling oxygenator ventilation. The mean paCO 2 value obtained during the study period was 39.0 +/-2.5 mmHg. There was no statistical difference between the paCO 2 values when separated into four different blood temperature groups, ( less than 28, 28-32, 32-37, and greater than 37 degrees C).     

Oxygenator exhaust capnography: a method of estimating arterial carbon dioxide tension during cardiopulmonary bypass.

An in vivo study was undertaken during hypothermic (28 degrees C) cardiopulmonary bypass to compare oxygenator exhaust capnography as a means of estimating arterial carbon dioxide tension (PaCO2) with bench blood gas analysis. A total of 123 pairs of measurements were made in 40 patients. Oxygenator exhaust capnographic measurements systematically underestimated PaCO2 measured by a bench blood gas analyzer. During the cooling and stable hypothermic phases of cardiopulmonary bypass, the relationship was reasonably accurate, but became far more variable during rewarming. Oxygenator exhaust capnography could be used as an inexpensive means of continuously monitoring PaCO2 during the cooling and stable hypothermic phases of cardiopulmonary bypass but should not be used during rewarming.     

The relationship between oxygenator exhaust P(CO2) and arterial P(CO2) during hypothermic cardiopulmonary bypass

During cardiopulmonary bypass the partial pressure of carbon dioxide in oxygenator arterial blood (P(a)CO2) can be estimated from the partial pressure of gas exhausting from the oxygenator (P(E)CO2). Our hypothesis is that P(E)CO2 may be used to estimate P(a)CO2 with limits of agreement within 7 mmHg above and below the bias. (This is the reported relationship between arterial and end-tidal carbon dioxide during positive pressure ventilation in supine patients.) During hypothermic (28-32 degrees C) cardiopulmonary bypass using a Terumo Capiox SX membrane oxygenator, 80 oxygenator arterial blood samples were collected from 32 patients during cooling, stable hypothermia, and rewarming as per our usual clinical care. The P(a)CO2 of oxygenator arterial blood at actual patient blood temperature was estimated by temperature correction of the oxygenator arterial blood sample measured in the laboratory at 37 degrees C. P(E)CO2 was measured by connecting a capnograph end-to-side to the oxygenator exhaust outlet. We used an alpha-stat approach to cardiopulmonary bypass management. The mean difference between P(E)CO2 and P(a)CO2 was 0.6 mmHg, with limits of agreement (+/-2 SD) between -5 to +6 mmHg. P(E)CO2 tended to underestimate P(a)CO2 at low arterial temperatures, and overestimate at high arterial temperatures. We have demonstrated that P(E)CO2 can be used to estimate P(a)CO2 during hypothermic cardiopulmonary bypass using a Terumo Capiox SX oxygenator with a degree of accuracy similar to that associated with the use of end-tidal carbon dioxide measurement during positive pressure ventilation in anaesthetized, supine patients.     

Oxygenator exhaust capnography for prediction of arterial carbon dioxide tension during hypothermic cardiopulmonary bypass

Continuous monitoring and control of arterial carbon dioxide tension (P(a)CO2) during cardiopulmonary bypass (CPB) is essential. A reliable, accurate, and inexpensive system is not currently available. This study was undertaken to assess whether the continuous monitoring of oxygenator exhaust carbon dioxide tension (PexCO2) can be used to reflect P(a)CO2 during CPB. A total of 33 patients undergoing CPB for cardiac surgery were included in the study. During normothermia (37 degrees C) and stable hypothermia (31 degrees C), the values of PexCO2 from the oxygenator exhaust outlet were monitored and compared simultaneously with the P(a)CO2 values. Regression and agreement analysis were performed between PexCO2 and temperature corrected-P(a)CO2 and temperature uncorrected-P(a)CO2. At normothermia, a significant correlation was obtained between PexCO2 and P(a)CO2 (r = 0.79; p < 0.05); there was also a strong agreement between PexCO2 and P(a)CO2 with a gradient of 3.4 +/- 1.9 mmHg. During stable hypothermia, a significant correlation was obtained between PexCO2 and the temperature corrected-P(a)CO2 (r = 0.78; p < 0.05); also, there was a strong agreement between PexCO2 and temperature corrected-P(a)CO2 with a gradient of 2.8 +/- 2.0 mmHg. During stable hypothermia, a significant correlation was obtained between PexCO2 and the temperature uncorrected-P(a)CO2 (r = 0.61; p < 0.05); however, there was a poor agreement between PexCO2 and the temperature uncorrected-P(a)CO2 with a gradient of 13.2 +/- 3.8 mmHg. Oxygenator exhaust capnography could be used as a mean for continuously monitoring P(a)CO2 during normothermic phase of cardiopulmonary bypass as well as the temperature-corrected P(a)CO2 during the stable hypothermic phase of CPB.     

Temperature-related differences in mean expired pump and arterial carbon dioxide in patients undergoing cardiopulmonary bypass

OBJECTIVE: To investigate the relationship between arterial carbon dioxide (PaCO(2)) and mean expired pump CO(2) during cardiopulmonary bypass (PeCPBCO(2)) in patients undergoing cardiac surgery with CPB during steady state, cooling, and rewarming phases of CPB. DESIGN: Consenting patients, prospective study. SETTING: University-affiliated hospital. PARTICIPANTS: Twenty-nine patients. INTERVENTIONS: Patients aged 22 to 81 years were enrolled. An alpha-stat acid-base regimen was performed during CPB. The PeCPBCO(2) was measured by an infrared multigas analyzer with the sampling line connected to the scavenging port of the oxygenator. Values for PaCPBCO(2) from the arterial outflow to the patient and PeCPBCO(2) during CPB at various oxygenator arterial temperatures were collected and compared. Data were analyzed by analysis of variance with 1-way repeated measures and post hoc pair-wise Tukey testing when appropriate. The differences between PaCPBCO(2) and PeCPBCO(2) were linearly regressed against temperature. A p value <0.05 was considered significant. MEASUREMENTS AND MAIN RESULTS: Three to 5 data sets during CPB were collected from each patient. The mean gradient between PaCPBCO(2) and PeCPBCO(2) was positive 12.4 +/- 10.0 mmHg during the cooling phase and negative 9.3 +/- 9.9 mmHg during the rewarming phase, respectively. On regression of the data, the difference between PaCPBCO(2) and PeCPBCO(2) shows a good correlation with the change in temperature (r(2) = 0.79). The arterial CO(2) +/- x mmHg can be predicted by the formula PaCPBCO(2) = (-2.17x + 69.2) + PeCPBCO(2), where x is temperature in degrees C. CONCLUSIONS: Monitoring the mean expired CO(2) value from the CPB oxygenator exhaust scavenging port with a capnography monitor provides a continuous and noninvasive data source to aid in sweep flow CPB circuit management during CPB.     

Cerebral carbon dioxide reactivity during nonpulsatile cardiopulmonary bypass

Five patients undergoing extensive cerebral monitoring during cardiopulmonary bypass (CPB) procedures were subjected to studies on cerebral CO2 reactivity during nonpulsatile CPB. The cerebral monitoring included recording of arterial blood pressure (BP), central venous pressure (CVP), epidural intracranial pressure (EDP), cerebral electrical activity by a cerebral function monitor (CFM), and middle cerebral artery (MCA) flow velocity by transcranial Doppler technique. The cerebral perfusion pressure (CPP) was thus continuously recorded (CPP = BP - EDP). During steady-state CPB with constant hematocrit, temperature, and arterial carbon dioxide tension (PaCO2), MCA flow velocity varied with changing CPP in a pressure-passive manner, indicating that the cerebral autoregulation was not operative. During moderately hypothermic (28 to 32 degrees C), nonpulsatile CPB, with steady-state hematocrit, temperature, and pump flow, we deliberately and rapidly changed PaCO2 for periods of 1 or 2 minutes by increasing gas flow to the membrane oxygenator, thereby testing the cerebral CO2 reactivity. Nineteen CO2 reactivity tests, performed at CPP levels ranging from 17 to 75 mm Hg, disclosed that the cerebral CO2 reactivity decreased with CPP, especially with CPP levels below 35 mm Hg. In these patients, concomitant changes in CPP during the CO2 reactivity test could be compensated for by adjusting the observed change in MCA flow velocity. The corrected CO2 reactivity values obtained in this way ranged from below 1.0 (observed at CPP levels below 20 mm Hg) to a 3.0 to 4.5% X mm Hg-1 change in PaCO2 (observed at CPP levels above 35 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of endtidal CO2 and arterial blood gas analysis in paediatric patients undergoing controlled ventilation with a laryngeal mask or a face mask

Endtidal CO2 (PECO2) and arterial blood gas tensions were compared between laryngeal mask (LMA) and face mask (FM) ventilation in paediatric outpatients. Following premedication with midazolam, anaesthesia was induced with either thiopentone or isoflurane and atracurium. Anaesthesia was maintained with N2O, O2 and isoflurane. Manually controlled ventilation was applied with a nonrebreathing system. Both PECO2 and arterial blood gas tensions were measured at 5 and 15 min after skin incision. The mean PaCO2 values in the LMA group were 36.6+/-7.4 and 37.5+/-6.4 mmHg and PaCO2 -PECO2 were 1. 8+/-2.4 and 2.5+/-3.3 mmHg, respectively. The mean PaCO2 values in the FM group were 41.3+/-8.1 and 43.4+/-8.9 mmHg; and PaCO2 -PECO2 were 5.3+/-3.6 and 8.8+/-7.0 mmHg, respectively. These values were lower in the LMA group (P< 0.05). We have concluded that monitoring of PECO2 is more reliable for estimating blood gas values during controlled ventilation with a LMA than a face mask.     

Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management

Twenty-eight adult patients anesthetized with fentanyl, then subjected to hypothermic cardiopulmonary bypass (CPB), were studied to determine the effect of phenylephrine-induced changes in mean arterial pressure (MAP) on cerebral blood flow (CBF). During CPB patients managed at 28 degrees C with either alpha-stat (temperature-uncorrected PaCO2 = 41 +/- 4 mmHg) or pH-stat (temperature-uncorrected PaCO2 = 54 +/- 8 mmHg) PaCO2 for blood gas maintenance received phenylephrine to increase MAP greater than or equal to 25% (group A, n = 10; group B, n = 6). To correct for a spontaneous, time-related decline in CBF observed during CPB, two additional groups of patients undergoing CPB were either managed with the alpha-stat or pH-stat approach, but neither group received phenylephrine and MAP remained unchanged in both groups (group C, n = 6; group D, n = 6). For all patients controlled variables (nasopharyngeal temperature, PaCO2, pump flow, and hematocrit) remained unchanged between measurements. Phenylephrine data were corrected based on the data from groups C and D for the effect of diminishing CBF over time during CPB. In patients in group A CBF was unchanged as MAP rose from 56 +/- 7 to 84 +/- 8 mmHg. In patients in group B CBF increased 41% as MAP rose from 53 +/- 8 to 77 +/- 9 mmHg (P less than 0.001). During hypothermic CPB normocarbia maintained via the alpha-stat approach at a temperature-uncorrected PaCO2 of approximately equal to 40 mmHg preserves cerebral autoregulation; pH-stat management (PaCO2 approximately equal to 57 mmHg uncorrected for temperature, or 40 mmHg when corrected to 28 degrees C) causes cerebrovascular changes (i.e., impaired autoregulation) similar to those changes produced by hypercarbia in awake, normothermic patients.     

Analysis of factors related to jugular venous oxygen saturation during cardiopulmonary bypass

OBJECTIVE: To investigate preoperative clinical conditions and/or intraoperative physiologic variables related to jugular venous oxygen saturation (SjO2) during cardiopulmonary bypass (CPB). DESIGN: Prospective study. SETTING: General hospital, single institution. PARTICIPANTS: One hundred forty patients (52 women, 88 men) who underwent coronary artery bypass grafting. MEASUREMENTS AND MAIN RESULTS: The authors measured SjO2 at five times during surgery. Multiple stepwise regression analysis showed a significant correlation of SjO2 with (1) arterial carbon dioxide partial pressure (PaCO2) before CPB (standard regression coefficient [(SC)] = 0.435), (2) cerebral perfusion pressure (CPP) during initiation of CPB (SC = 0.259), (3) PaCO2, tympanic temperature (TT), bubble oxygenator, and cerebral small infarctions (CSIs) during hypothermic CPB (SC = 0.507, -0.237, -0.192, and -0.189, respectively), (4) CPP, PaCO2, CSIs, and bubble oxygenator during rewarming (SC = 0.476, 0.294, -0.220, and -0.189, respectively), and (5) PaCO2 after CPB (SC = 0.480; p < 0.01). Correlation coefficients between SjO2 and CPP during rewarming were 0.40 (0.46 without CSI and 0.37 with CSI; p < 0.01). These results indicate that the relationship between CPP and SjO2 was significant in patients with CPP less than 40 mmHg during rewarming. CONCLUSION: During rewarming, when cerebral perfusion and oxygen demand change abruptly, but not during stable hypothermic CPB, CPP was a significant factor related to sjO2.     

The alveolar-arterial difference in oxygen tension increases with temperature-corrected determination during moderate hypothermia

Moderate hypothermia (32-33 degrees C) occurs in anesthetic practice. However, intrapulmonary gas exchange and the effect of temperature correction of blood gases on oxygen and carbon dioxide exchange have not been investigated in these patients. We investigated alveolar-arterial difference in oxygen tension (AaDO2) and arterial to end-tidal difference in carbon dioxide (Pa-ETCO2) during rewarming of eight ASA physical status I patients from hypothermia of 32 degrees C. Anesthesia was maintained with fentanyl/propofol. AaDO2 and Pa-ETCO2 were assessed by analyzing arterial blood gases and saturated water vapor pressure, uncorrected or corrected to actual body temperature. The respiratory quotient (RQ) was measured by calorimetry. After temperature correction of blood gases and water vapor pressure, the AaDO2 was significantly higher at 33 and 32 degrees C compared with 36 degrees C (56 +/- 13 and 64 +/- 14 vs 39 +/- 10 mm Hg; P < 0.05 and P < 0.01). The deterioration of pulmonary oxygen exchange was not detected if arterial blood gases and water vapor pressure were not corrected. The RQ did not change during moderate hypothermia compared with 36 +/-C. The temperature-corrected Pa-ETCO2 was not affected by hypothermia. We conclude that AaDO2 is increased during moderate hypothermia. This is only detected when water vapor pressure and arterial blood gases are corrected to actual body temperature. IMPLICATIONS: We investigated intrapulmonary oxygen and carbon dioxide exchange during moderate hypothermia (32 degrees C) in eight patients. If oxygen, carbon dioxide, and water vapor pressure were corrected to actual body temperature, the alveolar-arterial oxygen tension difference was increased during hypothermia. The carbon dioxide tension difference and the respiratory quotient were unaffected by hypothermia.     

A comparison of anaesthetic tensions in arterial blood and oxygenator exhaust gas during cardiopulmonary bypass

This study evaluates the usefulness of the analysis of gas sampled from the exhaust port of a membrane oxygenator in the estimation of anaesthetic tension in arterial blood. Sixty-seven arterial blood samples were drawn from patients undergoing hypothermic cardiopulmonary bypass with anaesthesia maintained by either isoflurane or desflurane. Anaesthetic tensions in the oxygenator exhaust gas were measured using an infrared analyser and in arterial blood using a two-stage headspace technique with a gas chromatograph. Both measurement systems were calibrated with the same standard gas mixtures. There was no difference in anaesthetic tension measured in arterial blood and gas leaving the oxygenator exhaust (isoflurane: n = 29, range: 0.3-0.8%, 95% limits of agreement: -0.08% to 0.09%; desflurane: n = 38, range: 1.5-5.4%; 95% limits of agreement -0.65% to 0.58%). We conclude that anaesthetic tensions in arterial blood can be accurately monitored by analysis of the gas emerging from the exhaust port of a membrane oxygenator.     

The reliability of endtidal CO2 in spontaneously breathing children during anaesthesia with laryngeal mask airway,low flow,sevoflurane and caudal epidural

BACKGROUND: Noninvasive devices for monitoring endtidal CO2 (PECO2) are in common use in paediatric anaesthesia. Questions have been raised concerning the reliability of these devices in spontaneous breathing children during surgery. Our anaesthetic technique for elective infraumbilical surgery consists of spontaneous breathing through a Laryngeal Mask Airway (LMA), low fresh gas flow, sevoflurane and a caudal epidural. We wanted to compare PECO2 and arterial CO2 (PaCO2) during surgery. METHODS: Twenty children, aged 1-6 years, scheduled for infraumbilical surgery, were studied and one arterial sample was taken 45 min after induction of anaesthesia. PECO2, inspiratory PCO2, oxygen saturation, heart rate, respiratory rate, mean arterial blood pressure and expiratory sevoflurane concentration were measured every 5 min. The respiratory and circulatory parameters were stable during surgery. RESULTS: The mean PaCO2 - PECO2 difference was 0.15 (0.16) kPa [1.1 (1.2 mmHg)]. CONCLUSIONS: PECO2 is a good indicator of PaCO2 in our anaesthetic setting.     

Cerebral blood flow response to PaCO2 during hypothermic cardiopulmonary bypass in rabbits

Differences in cerebral blood flow (CBF) between alpha-stat and pH-stat management depend on preserved responsiveness of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2). We tested the hypothesis that hypothermia-induced reductions in CBF would decrease the CBF response to changing PaCO2 (delta CBF/delta PaCO2). Anesthetized New Zealand white rabbits were randomly assigned to one of three temperature groups--group 1 (37 degrees C, n = 9); group 2 (31 degrees C, n = 10); or group 3 (25 degrees C, n = 10)--and were cooled using cardiopulmonary bypass. After esophageal temperature equilibration (approximately 40 min), oxygenator gas flows were serially varied to achieve PaCO2 values of 20, 40, and 60 mm Hg (temperature-corrected). All animals were studied at all three PaCO2 levels in random order. At each level of PaCO2, CBF and masseter blood flow were determined using radiolabeled microspheres. There were no significant differences between groups with respect to mean arterial pressure (approximately 80 mmHg), central venous pressure (approximately 4 mmHg), or hematocrit (approximately 22%). Prior normothermic studies have found delta CBF/delta PaCO2 to be proportional to CBF. Nevertheless, in this study, with hypothermia-induced reductions in CBF, delta CBF/delta PaCO2 was not significantly different between temperature groups. Thus, hypothermia either increased the sensitivity of the cerebral vasculature to carbon dioxide and/or increased the effective level of cerebrospinal fluid respiratory acidosis produced by each increment of temperature-corrected PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive intraoperative monitoring of carbon dioxide in children: endtidal versus transcutaneous techniques

BACKGROUND: The current study prospectively compares the accuracy of the intraoperative use of transcutaneous (Tc) and endtidal (PE) CO2 monitoring during surgical procedures in 30 paediatric patients, ranging in age from 6 months to 15 years (6.15 +/- 4.35 years) and in weight from 4.7 to 73 kg (24.9 +/- 18.2 kg). METHODS: Following calibration and an equilibration time for the TcCO2 monitor, arterial blood gas samples were obtained as clinically indicated. A total of 64 sample sets (PaCO2, PECO2 and TcCO2) were obtained from the 30 patients. RESULTS: The PECO2 to PaCO2 difference was 0.6-0.9 kPa (4.4 +/- 7.1 mmHg) while the TcCO2 to PaCO2 difference was 0.36-0.38 kPa (2.8 +/- 2.9 mmHg) (P=NS). The difference between the PaCO2 and PECO2 was 0.4 kPa (3 mmHg) or less in 37 of 64 sample sets while the difference between the PaCO2 and TcCO2 was 0.4 kPa (3 mmHg) or less in 49 of 64 sample sets (P=0.038). Linear regression analysis of PECO2 vs. PaCO2 revealed a slope of 0.434, r=0.8761, r2=0.7676. Linear regression analysis of TcCO2 vs. PaCO2 revealed a slope of 0.914, r=0.9472, r2=0.8972. CONCLUSIONS: Although in most circumstances, both noninvasive monitors of PCO2 provided a clinically acceptable estimate of PaCO2, TCCO2 provided a slightly more accurate estimate of PaCO2 during intraoperative anaesthetic care in children.     

Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog]

We investigated the effects of arterial carbon dioxide tension on the myocardial tissue oxygen tensions of subepicardium and subendocardium in the anesthetized dogs. The study was done in fourteen open-chest mongrel dogs, weighing 13 +/- 1 kg, anesthetized with sodium pentobarbital (30 mg.kg-1 iv), and mechanically ventilated with 100% oxygen to maintain normocapnia. End tidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode. Two pairs of combined needle sensors were carefully inserted, one in the epicardial and the other in the endocardial layer of the beating heart. Electromagnetic blood flow probe was applied on the left anterior descending artery (LAD). After a stable normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and this mechanical hyperventilation was kept fixed throughout the experiments. To induce hypercapnia, exogenous carbon dioxide was added to the inspired gas step-wise until FECO2 reached 10%. Hypocapnic hyperventilation (PaCO2: 22 mmHg) invariably resulted in a significant reduction of coronary blood flow (LADBF) and left ventricular myocardial tissue PO2 in both epicardial and endocardial layers, while addition of carbon dioxide to the inspired gas (hypercapnic hyperventilation) reversed the change by increased LADBF and arterial PaCO2 in a dose-dependent manner. These results indicate that injudicious and severe hypocapnic hyperventilation may induce impaired myocardial tissue perfusion and oxygenation although normal cardiac output and arterial blood oxygenation are maintained.     

Alterations in brain electrical activity may indicate the onset of malignant hyperthermia in swine

The time course of changes in brain electrical activity during halothane anesthesia was examined in 12 malignant hyperthermia-susceptible (MHS) and 14 normal (nMHS) swine. Power densities in selected frequency bands were calculated from the electroen-cephalogram (EEG). EEG and systemic variables were determined over a period of 60 min after starting halothane (1% inspired). Malignant hyperthermia (MH) was triggered in all susceptible pigs. Initial changes in the EEG during development of MH consisted of a decrease in total power and a shift to lower frequencies (delta-theta activity) in all animals. These EEG alterations were noted when there was an increase in heart rate, but other systemic variables were still normal. EEG changes in all MHS animals started at an arterial oxygen tension (PaO2) greater than 90 mmHg and an arterial carbon dioxide tension (PaCO2) less than 50 mmHg. In 5 MHS animals EEG became isoelectric at a PaO2 of 61-82 mmHg and a PaCO2 of 53-68 mmHg. Mean arterial blood pressure at this time was 54-66 mmHg. To determine the effects of hypoxia on the EEG in 7 nMHS animals, oxygen was decreased over a period of 45-60 min to 7% inspired. In 7 other nMHS animals, hypercarbia was produced by admixture of carbon dioxide to the fresh gas supply to achieve incremental increases of PaCO2 to 110-120 mmHg. Significant EEG changes during hypoxia comparable to those seen at the onset of MH were noted at a PaO2 below 40 mmHg and during hypercarbia at a PaCO2 greater than 68 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Bain anaesthetic circuit.

The Bain co-axial circuit is a recent and versatile addition to the semiclosed anaesthetic breathing systems. The relationship between the patient's arterial carbon dioxide tension (PaCO2) and fresh gas flow during intermittent positive pressure ventilation (IPPV) using this circuit has been reassessed. A mean PaCO2 of 33,4 mmHg for 64 patients was recorded using a fresh gas flow of 100 ml/kg/min and a mean PaCO2 of 37,3 mmHg for 55 patients using a fresh gas flow off 70 ml/kg/min.     

Differences in cerebral blood flow between alpha-stat and pH-stat management are eliminated during periods of decreased systemic flow and pressure. A study during cardiopulmonary bypass in rabbits

Prior reports suggest cerebral blood flow (CBF) responses to changing bypass (systemic) flow rates may differ between alpha-stat and pH-stat management. To compare the effect of blood gas management upon CBF responses to changing systemic flow and pressure, 15 New Zealand White rabbits, anesthetized with fentanyl and diazepam, underwent nonpulsatile cardiopulmonary bypass at 25 degrees C. One group of animals (n = 8) was randomized to alpha-stat blood gas management that maintained arterial carbon dioxide tension (PaCO2) approximately 40 mmHg when measured at 37 degrees C. A second group (n = 7) was managed with pH-stat technique, maintaining PaCO2 approximately 40 mmHg when corrected to the animal's actual temperature. Bypass was initiated at a flow rate of 100 ml.kg-1.min-1 and, after approximately 20 min, control hemodynamic and CBF measurements (radioactive microspheres) were made. Thereafter, bypass flow rate was changed in random order at 15-min intervals to 50, 70, and 100 ml.kg-1.min-1. CBF and hemodynamic measurements were repeated at the end of each period of altered bypass flow. Groups differed significantly with respect to both pHa and PaCO2. There were no significant differences between groups with respect to bypass flow rate, mean arterial pressure (MAP), central venous pressure, temperature, hematocrit, arterial oxygen tension (PaCO2), or bypass duration at any measurement point. MAP decreased significantly, from approximately 80 to approximately 65 mmHg with decreasing bypass flow (P = 0.0001). Over the entire range of bypass flows, CBF decreased with decreasing bypass flow (P = 0.001), and the degree of change was equivalent among regions and between groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rat cardiopulmonary bypass model: application of a miniature extracorporeal circuit composed of asanguinous prime

A clinically relevant rat cardiopulmonary bypass (CPB) model would be a valuable tool for investigating pathophysiological and therapeutic strategies on bypass. Previous rat CPB models have been described in the literature; however, they have many limitations, including large circuit surface area, the inability to achieve full bypass, and donor blood requirements for prime. Therefore, we have established a rat CPB model designed to overcome these limitations. The miniature circuit consisted of a filtered reservoir, heat exchanger, membrane oxygenator (surface area = 0.02 m2) with a static priming volume of 2.8 mL, and an inline blood gas monitor. The circuit was primed with 9.5+/-0.5 mL of crystalloid solution and CPB was established on male Sprague-Dawley rats (430-475 g, n = 5) by cannulating the left common carotid artery and the right external jugular vein. The animals were placed on CPB at full flow (111+/-13 mL/kg/ min) for 1 hour and were monitored for and additional 2 hours after the CPB procedure. Hemodynamics, hemoglobin concentration (Hb), and blood gases were analyzed at three time intervals: before, during, and after CPB. The circuit performance was evaluated according to prime volume, compliance, hemodynamic parameters, and gas and heat exchange as described by modified AMMI standards. Data are expressed as mean+/-SD and a repeated-measures analysis of variance with post-Hoc test was used for data comparison between the three time intervals. The ratio of oxygenator surface area to subject body weight for this model is comparable with that of current human adult CPB practice (0.05 m2/kg vs 0.057 m2/kg) Full CPB was achieved and we observed clinically acceptable PaO2, PaCO2, and SvO2 values (209+/-86 mmHg, 25+/-2 mmHg, 78+/-8%, respectively) while on CPB. The use of asanguinous prime did produce statistically significant Hg reduction (15.7+/-0.76 vs. 9.2+/-0.59 g/dL) comparable with clinical practice. No statistically significant differences between pre- and post-CPB hemodynamics and blood gases were found in our study. We have established a miniature circuit consisting of asanquineous prime for a rat CPB model that maintains clinically acceptable results regarding hemodynamic parameters, blood gases, and hemodilution. This model would be valuable for further use in clinically relevant research studies.