Measurements Of PETCO2 Research Articles

Acetazolamide compromizes the measurement of petCO2 but not ptcCO2

University Clinic for Anesthesiology and Intensive Care Medicine, University Hospital Mannheim, Mannheim, Germany

The measurement of end-tidal carbon dioxide (PETCO2) is not a significant parameter to monitor in patients with severe traumatic brain injury

To evaluate the agreement between end-tidal carbon dioxide (PETCO2) and arterial CO2 (PaCO2) in patients with traumatic brain injury and to document the course of the (PaCO2-PETCO2) gradient over time. Twenty one traumatic brain injury patients (Coma Glasgow Scale < or = 8) were included in this prospective observational study over a period of six months. Simultaneous determinations of PaCO2 and PETCO2 (by infrared capnometry) were recorded. Agreement between PaCO2 and PETCO2 was determined by the statistical method described by Bland and Altman. Changes in PETCO2 over time were compared with changes in PaCO2. Factors likely to explain a gradient superior to +/- 4 mmHg were explored. One hundred and eleven data pairs were obtained. The bias was 5.5 mmHg with a precision of 5.1 mmHg and limits of agreement ranged from -4.5 mmHg to 15.5 mmHg. The latter exceeded the predefined limits of agreement established to determine interchangeability between methods (+/- 4 mmHg). PETCO2 and PoCO2 changed in opposite directions in 20% of 90 consecutive measurements. Only the duration of ventilation was found to be significantly associated with a gradient superior to +/- 4 mmHg. In this selected population of patients with severe traumatic brain injury, measurements of PETCO2 and PaCO2 are not interchangeable. Further the PoCO2-PETCO2 gradient is not stable over time and cannot predict variations of PaCO2. The use of PETCO2 instead of PaCO2 could be deleterious in patients in whom strict control of PaCO2 values is required.

End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock.

To document the relationships between cardiac index and end-tidal carbon dioxide tension (PetCO2 during diverse low-flow states of circulatory shock. Randomized, prospective, controlled studies on animal models of hemorrhagic, septic, and cardiogenic shock. University-affiliated research laboratory. Sixteen anesthetized domestic pigs weighing 35-45 kg. Hemorrhagic shock was induced in five pigs by bleeding followed by reinfusion of shed blood. Septic shock was induced in five pigs by infusion of live Escherichia coli. Cardiogenic shock followed an interval of global myocardial ischemia after inducing and reversing ventricular fibrillation in six pigs. PetCO2 was continuously measured. Cardiac index was measured intermittently by using conventional thermodilution techniques. Cardiac index was correlated with PetCO2 by polynomial regression and Bland-Altman analyses. PetCO2 was highly correlated with cardiac index during hemorrhagic shock (r2 = .69, p < .01), septic shock (r2 = .65, p < .01), and cardiogenic shock (r2 = .81, p < .01). PetCO2 predicted thermodilution cardiac index with bias of -11+/-27 (+/-2 SD) mL/min/kg during hemorrhagic shock, 1.3+/-20.4 (+/- 2 SD) mL/min/kg during septic shock, and -1+/-12 (+/-2 SD) mL/min/kg during cardiogenic shock. Cardiac output and PetCO2 were highly related in diverse experimental models of circulatory shock in which cardiac output was reduced by >40% of baseline values. Therefore, measurement of PetCO2 is a noninvasive alternative for continuous assessment of cardiac output during low-flow circulatory shock states of diverse causes.

A PRELIMINARY REPORT ON THE POSTOPERATIVE RESPIRATORY EFFECTS FOLLOWING A SINGLE EPIDURAL DOSE OF SUSTAINED-RELEASE ECAPSULATED MORPHINE (C0401)*

S232 INTRODUCTION: DepoFoam[trade mark sign] drug delivery technology (DepoTech Corp.) consists of lipid based, spherical, multivesicular particles used to encapsulate water-soluble, water-stable compounds. A sustained-release encapsulated morphine (C0401) was recently developed for epidural administration to provide prolonged postoperative analgesia [1]. A dose-escalating phase I study in healthy volunteers demonstrated significant respiratory depression in some subjects at a 40 mg dose. In this phase II open-label study, 2 cohorts of 5 patients each are to receive 20 or 30 mg of epidural C0401 in ascending fashion. This study investigated the respiratory effects of lower C0401 doses as part of the safety and efficacy evaluation of this drug. METHODS: To date 4 patients, scheduled for total hip arthroplasty under regional anesthesia, consented for this IRB approved study. A 20 mg dose of C0401 was injected in the lumbar epidural space over 15 seconds. The epidural catheter was removed and the interspace, 1 level caudad from the epidural placement, was identified and bupivacaine injected intrathecally for surgical anesthesia. Postoperatively, selected respiratory variables were continuously monitored: nasal capnometry for end tidal PCO2 (PET CO2), respiratory rate (RR), and pulse oximetry (SpO2) on room air FIO2. All measurements were recorded after a 5 min observation period and confirmation of a plateau waveform for PET CO2 measurement. PCA fentanyl and acetaminophen with codeine were available for additional analgesia. RESULTS: Patients' mean (+/- SD) age, height and weight were 46 +/- 10 years, 170 +/- 6.6, cm and 71 +/- 13 kg respectively. Mean RR and PET CO2 are presented in the figure. The lowest RR and SpO2 values recorded were 8 breaths/min and 94% respectively. Those occurred postoperatively within the first 8 hr post C0401 dose. DISCUSSION: In this small patient sample 20 mg of C0401 did not cause any adverse respiratory events. PET CO2 and RR remained in acceptably safe ranges. PET CO2 increases were most notable between 5 and 8 hr postoperatively. Respiratory rate did not show a similar trend which may be explained by a decreased tidal volume. The lower RR and SpO2 values were transient and SpO2 could be maintained at 98-100% with low flow nasal oxygen administration.

Capnography Monitoring During Neurosurgery

In neurosurgery, estimation of PaCO2 from PETCO2 has been questioned. The aim of this study was to reevaluate the accuracy of PETCO2 in estimating PaCO2 during neurosurgical procedures lasting >3 h and to measure the effect of surgical positioning on arterial to end-tidal CO2 gradient (P[a-ET]CO2) over time. One hundred four neurosurgical patients classified into four groups (supine [SP], lateral [LT], prone [PR], sitting [ST]) were included in a prospective study. PaCO2, PETCO2, and P(a-ET)CO2 were measured after induction of anesthesia (T0), after positioning (T1), each following hour (T2, T3, T4), and at the end of the procedure after return to the SP position (T5). Data are expressed as the mean +/- SD, and statistical analysis used linear regression, the Bland-Altman method, and analysis of variance. The mean durations of positioning and surgery were 4.1+/-1 h and 3.7+/-1.3 h, respectively. We performed 624 simultaneous measurements of PaCO2 (33+/-5 mm Hg) and PETCO2 (27+/-4 mm Hg), leading to a mean P(a-ET)CO2 of 6+/-4 mm Hg. P(a-ET)CO2 of the LT group (7+/-3 mm Hg) was larger (compared with the SP, PR, and ST groups) because of a lower PETCO2 (26+/-4 mm Hg). Negative P(a-ET)CO2 (PETCO2 > PaCO2) occurred 22 times, only in the SP (n = 9) and ST groups (n = 13). Changes in opposite directions of PETCO2 and PaCO2 between two successive measurements were found in 26% of the cases. Correlation coefficients in the four groups (PaCO2 versus PETCO2) were not in good agreement (0.46 to 0.62; P < 0.001). The mean bias was between 5 and 7 mm Hg. The superior (13-15 mm Hg) and inferior (-5 to 0 mm Hg) limits of agreement were too large to expect PETCO2 to replace PaCO2. In conclusion, during neurosurgical procedures of >3 h, capnography should be performed with regular analysis of arterial blood gases for optimal ventilator adjustment. This study, which aimed to reevaluate the ability of PETCO2 to estimate PaCO2 during neurosurgical procedures according to surgical position, indicates that PETCO2 cannot replace PaCO2 for the following reasons: scattering of individual values; occurrence of negative arterial to end-tidal CO2 gradient (P[a-ET]CO2; PaCO2 and PETCO2 variations in opposite directions; large changes in P(a-ET)CO2 between two samples; and instability of P(a-ET)CO2 over time.

Venous Gas Embolism???A Comparison of Carbon Dioxide and Helium in Pigs

RUDSTON-BROWN, BLAIR; DRAPER, PAUL N.; WARRINER, BRIAN; WALLEY, KEITH R.; PHANG, P. TERRY Author Information

-The effect of desflurane on cerebral blood flow velocity and cerebrovascular reactivity to CO2 in children-.

To assess in children with a transcranial Doppler the effect on cerebral blood flow velocities of desflurane, whose cerebral vasodilator effects have been studied in animals and in adults with intracranial lesions. Prospective clinical study. Ten healthy children, mean age: 3.4 yr, ASA physical class 1, undergoing minor urologic surgery, were included in this study. Induction was obtained with atropine 10 micrograms.kg-1, fentanyl 3 micrograms.kg-1 and propofol 3 mg.kg-1. Endotracheal intubation was facilitated by atracurium 0.3 mg.kg-1. Mechanical ventilation, with a 50% air/oxygen mixture was adjusted to achieve an end-tidal CO2 (PETCO2) level of 38 +/- 2 mmHg. Monitoring included measurement of mean arterial blood pressure (MAP), heart rate, PETCO2, SpO2 and end-tidal desflurane concentrations (FETDes). Mean blood flow velocities (Vmean) were measured in the middle cerebral artery using a bi-directional 2 MHz TCD system (EME-TC 2000 S). A first TCD measurement followed intubation (T1). Thereafter, desflurane was adjusted to 1 MAC. Six other TCDs were recorded each minute until FETDes reached the inspired fraction (T2-T7). Thereafter, CO2 reactivity was assessed with a hypocapnia test, induced by hyperventilation. Measures were done at T8 (PETCO2: 33 +/- 1 mmHg), T9 (PETCO2: 29 +/- 1 mmHg), and T10 (initial PETCO2: 38 +/- 1 mmHg). All these measurements were made before starting surgery. Analysis of variance (ANOVA) was used to analyse the data (P < 0.05 was considered as significant). The Vmean and heart rate increased significantly with increasing concentrations of desflurane (Vmean from 68 +/- 27 to 106 +/- 30 cm.s-1 and heart rate from 109 +/- 17 to 136 +/- 15 b.min-1 between T1 and T7). During hypocapnia, Vmean decreased to 68 +/- 23 cm.s-1 at T9, and returned to normal values with PETCO2 at 38 mmHg at T10. SpO2 remained unchanged. Mean arterial pressure was stable from T1 to T7, but decreased significantly at T9 and T10. Desflurane elicits a dose-dependent increase in cerebral blood flow velocities and heart rate, but does not change mean arterial pressure, suggesting that its cerebrovascular action is independent of its systemic vascular action. CO2 reactivity is maintained at one MAC. The results in children are similar to those seen in adults.

Clinical study of PEtCO2 in one-lung ventilation

Fourty-eight patients (ASA physical status I — I) undergoing selected thoracotomy and pulmonectomy were studied. They were divided into two groups according to different respiratory modes, two-lung ventilation (TLV) and onelung ventilation (OLV) or TLV and OLV with a Bain cyclic system for CPAP on the side of operated lung. PetCO2 and PaCO2 were measured after 30 min TLV, 30 min and 60 min OLV, and repeated TLV (R-TLV) 30 min after pulmonectomy, to evaluate the difference between PetCO2 and PaCO2 in OLV and to observe the effect of abating hypoxemia and discharge of CO2 in OLV with Bain system. Our results showed that the PaCO2 and PetCO2 in different test groups were normal though the measured values in OLV were slightly higher than that in TLV (P 0. 05). There was no significant difference between group 1. and 2. in OLV (P>0. 05). There was a close correlation between PetCO2 and PaCO2(P<0.05). The differences of the calculated P(a-et)CO2 and radio of PetCO2/ PaCO2 in different ventilation modes were not significant. Hypoxemia in OLV was corrected by Bain system, but the discharge of CO2 was not affected. The results showed that measurement of Pet CO2 as a non-invasive procedure can be commonly used to monitor OLV.

Carbon dioxide absorption during laparoscopic cholecystectomy and inguinal hernia repair

Laparoscopic surgical procedures require CO2 insufflation. The extent of CO2 absorption may differ with regard to the surgical technique used. The aim of this study was to quantify the CO2 absorption following intra- and extraperitoneal insufflation. The study was approved by the Ethics Committee and informed consent was obtained. Two groups of 25 ASA I and II patients each were prospectively studied: laparoscopic cholecystectomy (group A) and inguinal hernia repair (group B). All patients had no medical history of pulmonary or cardiac disease. All patients underwent the same standardized general anaesthesia. Following tracheal intubation, all patients were mechanically ventilated (RR=12 min−1; VT=8 ml kg−1). After 20 min (T1), baseline measurements of HB, BP, CVP, airway pressure, PET CO2 and oxygen saturation were performed and an arterial blood was sampled for gas analysis. Then, CO2 insufflation was started and the VT was adjusted to maintain PET CO2 at baseline level. After 20 min of insufflation (T2), all measurements and arterial blood gas sampling were repeated. The paired and unpaired Student's t-test was used to compare within and between groups respectively. Differences were considered significant at the P<0.01 level. Age in group A and B was 53 ± 13 and 60 ± 12 years respectively. Weight was 69 ± 9 (group A) and 72 ± 9.5 kg (group B). The comparison within groups at T1 and T2 revealed no significant differences for PET CO2, Pa CO2, HR and BP. In both groups, a statistically significant increase in peak airway pressure, CVP and VT was found. The increase in VT required to maintain normocapnia in group A was 30.9 ± 8.4% (from 556 ± 79 to 724 ± 84 mL), the required increase in group B was 55.4 ± 19.5% (from 592 ± 92 to 909 ± 104 mL). Statistical differences between groups were found for the increase in VT, CVP and airway pressure. This study provides evidence that extraperitoneal CO2 insufflation induces a greater CO2 absorption compared with intraperitoneal insufflation.

Do Changes in End-Tidal Pco2 Quantitatively Reflect Changes in Cardiac Output?

In anesthetized patients, acute decreases in cardiac output (CO) are often reflected as decreases in end-tidal CO2 tension (PETCO2), but the quantitative relationship between the changes in CO and the changes in PETCO2 is uncertain. We hypothesize that a quantitative relationship can be demonstrated if timing of the measurements in each episode of hemodynamic perturbation is standardized. In 24 patients undergoing abdominal aortic aneurysm surgery with constant ventilation, we prospectively performed 33 measurements of CO, PETCO2, and CO2 elimination (VECO2) within 10 min of hemodynamic changes. The percent decrease in PETCO2 directly correlated with the percent decrease in CO (slope = 0.33, r2 = 0.82). Also, the percent decrease in VECO2 correlated with the percent decrease in CO similarly (slope = 0.28, r2 = 0.84). The changes in PETCO2 and VECO2 following hemodynamic perturbation were parallel. This finding suggests that decreases in PETCO2 quantitatively reflect the decreases in CO2 elimination.

A comparison of transcutaneous, end-tidal and arterial measurements of carbon dioxide during general anaesthesia

A randomized, prospective study was performed to evaluate the accuracy of a new transcutaneous carbon dioxide (CO2) monitor (Fastrac) during general anaesthesia. Twenty-two adult patients undergoing elective surgery were subjected to three different levels of minute ventilation by varying their respiratory rates in a randomized cross-over design. Simultaneous measurements of transcutaneous CO2 (PTCCO2) and arterial CO2 (PaCO2) were obtained at three levels of minute ventilation (low, medium and high). End-tidal CO2 (PETCO2) values were also recorded from a mass spectrometer (SARA) at each time period. A total of 66 data sets with PaCO2 ranging from 28-62 mmHg were analyzed. The PTCCO2 values demonstrated a high degree of correlation with PaCO2 over the range of minute ventilation (y = 0.904x + 6.36, r = 0.92, P less than 0.001). The PETCO2 measurement also demonstrated a generally good correlation with PaCO2 (y = 0.62x + 9.21, r = 0.89, and P less than 0.01). However, the PETCO2-PaCO2 gradients (mean 7.0 +/- 3.1 mmHg) were greater than the PTCCO2-PaCO2 gradients (mean 2.3 +/- 2.4 mmHg) at all three levels of minute ventilation (P less than 0.05). These differences were greatest when PaCO2 was in the high range (48-60 mmHg). We conclude that the new Fastrac CO2 monitor is accurate for monitoring carbon dioxide levels during general anaesthesia. The new transcutaneous devices provide an effective method for non-invasive monitoring of CO2 in situations where continuous, precise control of CO2 levels is desired.

Cerebral Blood Flow Reactivity to Changes in Carbon Dioxide Calculated Using End-Tidal versus Arterial Tensions

We retrospectively examined arerial and end-tidal estimations of CO2 tension used to calculate cerebrovascular reactivity in 68 anesthetized patients. CBF was measured using the intravenous 133Xe technique at mean +/- SD PaCO2 values of 28.2 +/- 5.2 and 38.8 +/- 4.8 mm Hg. The correlation between all PaCO2 and end-tidal PCO2 (PetCO2) values was y = 0.85x - 0.49 (r = 0.93, p = 0.0001). There was a moderate correlation between age and the difference between PaCO2 and PetCO2 (y = 0.11x + 0.79; r = 0.73, p = 0.0001). Cerebrovascular reactivity to changes in CO2 (ml 100 g-1 min-1 mm Hg-1) was similar (p = 0.358) when calculated by using either PaCO2 (1.9 +/- 0.8) or PetCO2 (1.8 +/- 0.8) and highly correlated (y = 0.86x + 0.23; r = 0.91, p = 0.0001). The CBF response to changes in CO2 tension can be reliably estimated from noninvasive measurement of PetCO2.

Accuracy of end-tidal carbon dioxide tension analyzers

Substantial mean differences between arterial carbon dioxide tension (PaCO2) and end-tidal carbon dioxide tension (PETCO2) in anesthesia and intensive care settings have been demonstrated by a number of investigators. We have explored the technical causes of error in the measurement of PETCO2 that could contribute to the observed differences. In a clinical setting, the measurement of PETCO2 is accomplished with one of three types of instruments, infrared analyzers, mass spectrometers, and Raman spectrometers, whose specified accuracies are typically +/- 2, +/- 1.5, and +/- 0.5 mm Hg, respectively. We examined potential errors in PETCO2 measurement with respect to the analyzer, sampling system, environment, and instrument. Various analyzer error sources were measured, including stability, warm-up time, interference from nitrous oxide and oxygen, pressure, noise, and response time. Other error sources, including calibration, resistance in the sample catheter, pressure changes, water vapor, liquid water, and end-tidal detection algorithms, were considered and are discussed. On the basis of our measurements and analysis, we estimate the magnitude of the major potential errors for an uncompensated infrared analyzer as: inaccuracy, 2 mm Hg; resolution, 0.5 mm Hg; noise, 2 mm Hg; instability (12 hours), 3 mm Hg; miscalibration, 1 mm Hg; selectivity (70% nitrous oxide), 6.5 mm Hg; selectivity (100% oxygen), -2.5 mm Hg; atmospheric pressure change, less than 1 mm Hg; airway pressure at 30 cm H2O, 2 mm Hg; positive end-expiratory pressure or continuous positive airway pressure at 20 cm H2O, 1.5 mm Hg; sampling system resistance, less than 1 mm Hg; and water vapor, 2.5 mm Hg. In addition to these errors, other systematic mistakes such as an inaccurate end-tidal detection algorithm, poor calibration technique, or liquid water contamination can lead to gross inaccuracies. In a clinical setting, unless the user is confident that all of the technical error sources have been eliminated and the physiologic factors are known, depending on PETCO2 to determine PaCO2 is not advised.

Acute chest pain without obvious organic cause before the age of 40 years: response to forced hyperventilation

A hyperventilation provocation test (HVPT) was performed on a group (n = 63) of consecutive patients, below the age of 40 years, attending an emergency care unit complaining of chest pain without obvious organic cause. The results were compared with those for a control group (n = 32). There was no tendency to hyperventilate in the patient group, either after discontinuing hyperventilation or during the ensuing relaxation period. PETCO2 measurements during this time thus showed no significant differences between the patient group and the control group. During the HVPT, 44% of patients reported three or more listed symptoms familiar to them from earlier occasions and regarded as typical of hyperventilation, compared to 23% of the controls (P less than 0.05). In a previously reported study, 38% of the patients were found to have similar symptoms during standardized mental stress, despite lack of hypocapnia. It is concluded that, on the basis of PETCO2 measurements, there were no signs of abnormal hyperventilation in the patient group. Moreover, the HVPT did not appear to be specific for diagnosis of hyperventilation syndrome, since mental stress itself was able to reproduce symptoms without concomitant hypocapnia, and since the provocation test was 'positive' in many control subjects.

Comparison of arterial, end-tidal and transcutaneous PCO2 during moderate exercise and external C02 loading in humans

Static relationships between arterial, transcutaneous and end-tidal PCO2 (PaCO2, PtcCO2, PetCO2) as well as the dynamic relationship between PetCO2 and PtcCO2 were studied during moderate bicycle ergometer exercise with and without external CO2 loading. The exercise pattern consisted of 5-min intervals of constant power at 40 W and 100 W and 900 s of randomised changes between these two power levels. The external CO2 loading was achieved by means of controlled variations of inspiratory gas compositions aimed at a constant PetCO2 of 6.5 kPa (49 mm Hg). The PetO2 was regulated at 17.3 kPa (130 mm Hg). Under steady-state conditions all PCO2 parameters showed close linear relationships. PaCO2/PtcCO2 was near to identity while the PetCO2 systematically overestimated changes in PaCO2l No relationship showed a significant influence of the exercise intensity. Transients of PtcCO2 are considerably slower than PetCO2 transients. The dynamic relationship between both parameters was found to be independent of whether internal or external CO2 loadings were applied. It is concluded that the combination of PetCO2 and PtcCO2 measurements allows an improved non-invasive assessment of PaCO2. While PetCO2 better reflects the transients, PtcCO2 can be employed to determine slow changes of the absolute PaCO2.

Ventilatory Effects of Laparoscopy Under Epidural Anesthesia

This study evaluates the respiratory effects of laparoscopy under epidural anesthesia in seven female patients (ASA physical status I) scheduled for a gamete intrafallopian transfer procedure. Epidural anesthesia was performed with 15-18 mL of 1.5% plain lidocaine using a catheter inserted at the L3-4 level. The upper level of analgesia to pinprick was measured 20 min after lidocaine injection. Ventilatory measurements and arterial blood gas analyses were performed (a) preoperatively, in the horizontal supine position with a T7-9 level of analgesia; (b) in the 20 degrees Trendelenburg position with a T2-5 level of analgesia; (c) during intraabdominal insufflation of CO2 through the laparoscope; and (d) after CO2 exsufflation by manual compression of the abdomen before removal of the laparoscope while in the horizontal position. On-line measurements of VO2, VCO2, VE, VT, F, and PETCO2 were made using a Beckman metabolic cart, while the patients breathed room air through an anesthetic face mask. No significant changes in the ventilatory variables were observed in the Trendelenburg position. In contrast, CO2 insufflation significantly increased VE (from 9.1 +/- 1.0 L/min to 11.8 +/- 2.6 L/min, mean +/- SD), and F (from 16.9 +/- 1.9 breaths/min to 23.1 +/- 3.3 breaths/min, mean +/- SD), whereas VCO2 remained unchanged. PaCO2 remained constant throughout the study. These results suggest that epidural anesthesia may be a safe alternative to general anesthesia for outpatient laparoscopy, as it is not associated with ventilatory depression.

End-tidal carbon dioxide measurements in critically ill neonates: a comparison of side-stream and mainstream capnometers

To determine whether end-tidal PCO2 (PETCO2) measurements obtained with two infrared capnometers accurately approximates the arterial PCO2 (PaCO2) in critically ill neonates, simultaneous measurements of PETCO2 were obtained from the distal and proximal ends of the tracheal tube with a sidestream capnometer (Puritan Bennett/Datex--BP/D) and from the proximal end with a mainstream capnometer (Hewlett-Packard-HP) in 20 intubated neonates. Distal sidestream PETCO2 and mainstream PETCO2 correlated with the PaCO2 (r2 = 0.66 and 0.61, respectively) within the range of 26-57 mmHg PaCO2. However, proximal PETCO2 with the sidestream capnometer correlated very poorly (r2 = 0.09) with PaCO2. The slope of the least square regression line for the distal sidestream capnometer, 0.67, was significantly less than that for the mainstream capnometer, 0.78 but both were significantly greater than that for the proximal sidestream capnometer, 0.39 (P less than 0.05). The slope of the regression for the proximal sidestream capnometer did not differ significantly from horizontal. Insertion of the mainstream sensor for the HP capnometer significantly increased the transcutaneous CO2 when compared with preinsertion values. We conclude that both distal sidestream and mainstream capnometry provide accurate estimates of the PaCO2 in critically ill neonates.

Accuracy of end-tidal PCO2 measurements using a sidestream capnometer in infants and children ventilated with the Sechrist infant ventilator

To determine the accuracy of end-tidal PCO2 (PETCO2) measurements analyzed with a sidestream capnometer in infants and children whose lungs were ventilated with a Sechrist infant ventilator and an Ayre's t-piece, we compared PETCO2 measurements obtained from the proximal (PETCO2-p) and distal (PETCO2-d) ends of the tracheal tube to arterial PCO2 (PaCO2) in 37 healthy infants and children between 1.3 and 24.5 kg. Both PETCO2-p and PETCO2-d accurately approximated PaCO2, however, the mean (+/- SD) arterial to end-tidal PCO2 difference (delta(a-ET)PCO2) was significantly greater with proximal (1.27 +/- 1.54 mmHg) than with distal sampling (0.64 +/- 1.64 mmHg) (P less than 0.01). In the subgroup of patients who weighted less than 12 kg, the delta(a-ET)PCO2 using proximal gas sampling (1.94 +/- 1.29 mmHg) was also significantly greater than it was using distal sampling (0.74 +/- 1.31 mmHg) (P less than 0.001). We conclude that although statistically different, both proximal and distal estimates of PETCO2 provide acceptable estimates of PaCO2 in healthy infants and children who are ventilated with a Sechrist infant ventilator and an Ayre's t-piece system.

End tidal carbon dioxide as an haemodynamic determinant of cardiopulmonary resuscitation in the rat

End tidal PCO2 (PETCO2) has been found to be a good prognostic indicator of successful resuscitation from cardiac arrest. To explore the value of this measurement further, we carried out a series of experiments during cardiac arrest and closed chest resuscitation in 14 mechanically ventilated Sprague-Dawley rats. Ventricular fibrillation (VF) was induced by a 10 mA current delivered to the right ventricular endocardium. After 4 min of VF, precordial compression was begun with a mechanical thumper and defibrillation was attempted 2 min later. PETCO2 decreased abruptly during cardiac arrest to 0.3 mm Hg (0.04 kPa). With precordial compression, it increased to 11 mm Hg (1.5 kPa). Within 3 min of successful defibrillation, there was an overshoot in the PETCO2 to 44 mm Hg (5.8 kPa) with return to baseline levels approximating those of the pre-arrest control measurements over the 60 min that followed restoration of spontaneous circulation. The PETCO2 measurement during precordial compression predicted the success of defibrillation with return of spontaneous circulation. When PETCO2 exceeded 9 mm Hg (1.2 kpA), 7 of 8 animals were successfully resuscitated. When PETCO2 was less than 9 mm Hg during precordial compression, none of six animals were successfully resuscitated. The PETCO2 correlated with the mean aortic (r = 0.71) and coronary perfusion pressure (r = 0.80) generated during precordial compression. In corroboration of previously reported observations on pigs, dogs, and human patients, PETCO2 served as a non-invasive monitor of the effectiveness of precordial compression for maintaining coronary perfusion and therefore cardiac viability during CPR. The PETCO2 was also useful in that it promptly signalled restoration of spontaneous circulation.

Fresh gas formulae do not accurately predict end-tidal PCO2 in paediatric patients.

To determine the fresh gas flow (FGF) requirements in paediatric patients, we measured the FGFs needed to maintain distal end-tidal PCO2 (PETCO2) values at 30 and 38 mmHg in patients weighing between 3.8 and 20 kg ventilated with either a Sechrist Infant Ventilator IV-100B or an Air-Shields Ventimeter and a Mapleson D circuit. The FGF requirement was 500 ml.kg-1.min-1 to maintain a PETCO2 of 30 mmHg and 250 ml.kg-1.min-1 to maintain a PETCO2 of 38 mmHg when minute ventilation greater than or equal to FGF. When these formulae were used in a subsequent group of similar patients, a wide variation in PETCO2 measurements were obtained. We conclude that the safest and most accurate approach to determine the FGF requirement of paediatric patients is to continuously monitor the PETCO2 in each patient and to adjust the FGF accordingly.