Arterial to end-tidal carbon dioxide tension difference during anaesthesia for tubal ligation

Twenty-nine patients scheduled for postnatal tubal ligation by minilaparotomy under general anaesthesia were studied. Arterial and end-tidal carbon dioxide tensions were determined during anaesthesia. The mean arterial to end-tidal carbon dioxide tension difference was 0.08 kPa (SEM 0.05). Thirty-one percent of the patients had negative values. These results were similar to those observed during Caesarean section. The physiological changes responsible for reduced arterial to end-tidal carbon dioxide values, persist into the postnatal period. It is predicted from the regression analysis of the time between delivery and anaesthesia for tubal ligation and arterial to end-tidal CO2 difference, that the values might return to normal nonpregnant levels by 8 days following delivery.     

Arterial to end-tidal carbon dioxide tensio difference during laparoscopy Magnitude and effect of anaesthetic technique

The relationship between arterial carbon dioxide tension and end-tidal carbon dioxide tension was studied in 25 patients during laparoscopy. Thirteen patients received general anaesthesia and 12 epidural anaesthesia. The overall mean difference between arterial and end-tidal carbon dioxide tensions was 0.44 kPa (95% confidence intervals 0.28-0.60 kPa) which was significantly less than that reported in studies during other procedures. The reasons for this difference are probably associated with the physiological changes induced by CO2 pneumoperitoneum and steep Trendelenburg positioning. The choice of anaesthetic technique did not affect the arterial to end-tidal carbon dioxide tension difference significantly (p greater than 0.9).     

The influence of changes in end-tidal carbon dioxide upon the Bispectral Index

Carbon dioxide is known to affect consciousness in animals and humans. We surmised that changes in end-tidal carbon dioxide during anaesthesia might affect the Bispectral Index. Twenty-four patients due to undergo surgery were anaesthetised with fentanyl and a propofol infusion. The Bispectral Index, pulse rate and blood pressure were recorded while end-tidal carbon dioxide levels were changed. The patients acted as their own controls as they were subjected to high, normal and low levels of end-tidal carbon dioxide (3-12 kPa) according to a randomised sequence. There were no changes in the Bispectral Index or haemodynamic variables resulting from manipulation of the end-tidal carbon dioxide. At the level of hypnosis involved in this study, changes in end-tidal carbon dioxide, within the range tested, do not result in changes in the Bispectral Index.     

Accuracy of end-tidal carbon dioxide monitoring using the NBP-75 microstream capnometer. A study in intubated ventilated and spontaneously breathing nonintubated patients

Arterial carbon dioxide partial pressure measurements using the NBP-75 microstream capnometer were compared with direct PaCO2 values in patients who were (a) not intubated and spontaneously breathing, and (b) patients receiving intermittent positive pressure ventilation of the lungs and endotracheal anaesthesia. Twenty ASA physical status I-III patients, undergoing general anaesthesia for orthopaedic or vascular surgery were included in a prospective crossover study. After a 20-min equilibration period following the induction of general anaesthesia, arterial blood was drawn from an indwelling radial catheter, while the end-tidal carbon dioxide partial pressure was measured at the angle between the tracheal tube and the ventilation circuit using a microstream capnometer (NBP-75, Nellcor Puritan Bennett, Plesanton, CA, USA) with an aspiration flow rate of 30 mL min(-1). Patients were extubated at the end of surgery and transferred to the postanaesthesia care unit, where end-tidal carbon dioxide was sampled through a nasal cannula (Nasal FilterLine, Nellcor, Plesanton, CA, USA) and measured using the same microstream capnometer. In each patient six measurements were performed, three during mechanical ventilation and three during spontaneous breathing. A good correlation between arterial and end-tidal carbon dioxide partial pressure was observed both during mechanical ventilation (r = 0.59; P = 0.0005) and spontaneous breathing (r = 0.41; P = 0.001); while no differences in the arterial to end-tidal carbon dioxide tension difference were observed when patients were intubated and mechanically ventilated (7. 3 +/- 4 mmHg; CI95: 6.3-8.4) compared to values measured during spontaneous breathing in the postanesthesia care unit, after patients had been awakened and extubated (6.5 +/- 4.8 mmHg; CI95: 5. 2-7.8) (P = 0.311). The mean difference between the arterial to end-tidal carbon dioxide tension gradient measured in intubated and non-intubated spontaneously breathing patients was 1 +/- 6 mmHg (CI95: -11-+13). We conclude that measuring the end-tidal carbon dioxide partial pressure through a nasal cannula using the NBP-75 microstream capnometer provides an estimation of arterial carbon dioxide partial pressure similar to that provided when the same patients are intubated and mechanically ventilated.     

Malignant hyperthermia: advances in diagnostics and management

Real-time monitoring of end-tidal carbon dioxide during anaesthesia aids in the early detection of malignant hyperthermia and the occurrence of a rapid increase in end-tidal carbon dioxide, associated with unexplained persistent tachycardia, well before the core temperature begins to rise. Should malignant hyperthermia occur, however, dantrolene permits the dependable reversal of skeletal muscle hypermetabolism.     

Arterial to end-tidal carbon dioxide tension difference in children under halothane anaesthesia

Using blood gas determinations and capnography, the relationship between arterial and end-tidal PCO₂ was investigated in 20 children under halothane anaesthesia with spontaneous respiration. A median arterial to end-tidal carbon dioxide tension difference of 0.66 kPa (5 mm Hg) was found. There was a close correlation between Pa_co2 and the magnitude of the carbon dioxide difference. Our findings may largely be explained by an increase in Vd/Vt (presumably mainly due to a reduction of Vt) causing admixture of dead space air throughout expiration. It is concluded that though end-tidal carbon dioxide does not exactly reflect Pa_co2 capnography may be of value as a monitor of respiration in paediatric anaesthesia at normal or near-normal values of end-tidal carbon dioxide.     

Survey of use of end-tidal carbon dioxide for confirming tracheal tube placement in intensive care units in the UK

The use of end-tidal carbon dioxide monitoring to confirm the correct placement of a tracheal tube immediately after intubation is mandatory in the operating theatre. Tracheal intubation in critically ill patients can be challenging. Quick and accurate confirmation of tracheal tube placement is essential to minimise complications. This survey explored the use of end-tidal carbon dioxide monitoring to confirm tracheal tube placement in intensive care units in the UK. Questionnaires were sent to either the lead clinician or clinical director of randomly selected general adult intensive care units. One hundred and twenty-seven replies were received from the 215 questionnaires sent (response rate 59%). Twenty per cent of the units did not have an end-tidal carbon dioxide monitor, 20% had one end-tidal carbon dioxide monitor per bed and 60% had one end-tidal carbon dioxide monitor between several beds. Only 50% of the units having an end-tidal carbon dioxide monitor use it to confirm correct tracheal tube placement. Of these 50%, only about a third use it for every intubation. Seventy-two per cent of respondents felt that end-tidal carbon dioxide is well suited to confirm correct placement of tracheal tube in critically ill patients, but 50% did not think that confirmation using end-tidal carbon dioxide should be mandatory for intubations outside the operating theatre. Half of the units not having end-tidal a carbon dioxide monitor cited lack of resources as a reason. In summary, although four in every five intensive care units surveyed have end-tidal carbon dioxide monitors, only a small proportion use them to confirm correct placement of tracheal tube after intubation.     

Transcranial doppler: response of cerebral blood-flow velocity to carbon dioxide in anaesthetized children

To determine the effect of carbon dioxide on the cerebral circulation in anaesthetized infants and children, 13 healthy children, ASA physical status I or II, between three months and seven years of age and scheduled for urologic surgery, were studied. Anaesthesia was induced with thiopentone and vecuronium. After tracheal intubation, anaesthesia was maintained with 70 per cent nitrous oxide in oxygen, fentanyl 2 micrograms.kg-1, vecuronium 0.05 mg.kg-1 and 0.8-1.0 per cent end-tidal isoflurane. A caudal block was performed before surgery. Systolic arterial pressure, heart rate, oxygen saturation, temperature, and end-tidal isoflurane were maintained constant. Ventilation was adjusted to achieve an end-tidal PCO2 (PETCO2) of 20 mmHg. The PETCO2 was then randomly adjusted between 20 and 80 mmHg by the addition of carbon dioxide from an exogenous source. Cerebral blood flow velocity increased logarithmically and directly with the PETCO2 (r2 = 0.56). There were no complications associated with the use of transcranial Doppler sonography. These data indicate that CO2 has a direct effect on the velocity of blood in the middle cerebral artery in infants and children anaesthetized with isoflurane.     

Carbon dioxide output in laparoscopic cholecystectomy

In pneumoperitoneum, carbon dioxide eliminated in expired gas (carbon dioxide output) contains both metabolic and absorbed carbon dioxide from the peritoneal cavity. When elimination of carbon dioxide is much higher than carbon dioxide output, storage of tissue carbon dioxide and arterial carbon dioxide concentrations change. Finally, the rate of carbon dioxide eliminated in expired gas is not a match for the real rate of metabolic production and absorbed carbon dioxide from the peritoneal cavity. During and after insufflation of carbon dioxide, changes in carbon dioxide output were elucidated under constant arterial carbon dioxide pressure (PaCO2), the same as the preinduction level. We studied patients undergoing elective laparoscopic cholecystectomy. Carbon dioxide output, oxygen uptake, respiratory exchange ratio (RER), expired minute ventilation (VE), deadspace to tidal volume ratio (VD/VT ratio) and arterial to end-tidal carbon dioxide partial pressure difference (PaCO2-PE'CO2) were determined before induction, and during anaesthesia, pneumoperitoneum and recovery. By controlling ventilatory frequency (f) every 1 min, PaCO2 was adjusted to concentrations before induction. Constant monitoring of end-tidal carbon dioxide partial pressure (PE'CO2) and intermittent measurement of (PaCO2-PE'CO2) (15-min intervals) were conducted to predict PaCO2). Carbon dioxide output and oxygen uptake decreased significantly from mean values of 83.5 (SEM 5.2), 101.6 (5.1) to 68.5 (4.2), 81.1 (4.6) ml min-1 m-2 (ATPS, P < 0.05) with sevoflurane anaesthesia, and RER did not change. During carbon dioxide pneumoperitoneum (intra-abdominal pressure 8 mm Hg), carbon dioxide output increased by 49% (102.4 (5.0) ml min-1 m-2) (P < 0.05) while oxygen uptake remained stable and RER increased from 0.84 (0.02) to 1.16 (0.03) (P < 0.05). It was necessary to increase VE during pneumoperitoneum by 1.54 times that during anaesthesia to maintain individual PaCO2 values constant. After removal of carbon dioxide from the abdominal cavity, the regression equation of excess carbon dioxide output/BSA best fitted a two-compartment model. The time constants of the rapid and slow compartments were 8.2 and 990 min, respectively. Excess carbon dioxide output/BSA was still 5.5 ml min-1 m-2, 30 min after pneumoperitoneum.      

Mainstream vs. sidestream capnometry for prediction of arterial carbon dioxide tension during supine craniotomy

We compared the performance of mainstream capnometry as a measure of arterial carbon dioxide tension (Paco2) with sidestream recordings in adult neurosurgical patients undergoing supine craniotomy. Two hundred and forty patients were randomly assigned so that the end-tidal carbon dioxide tension (PEco2) was measured using either a mainstream or sidestream infrared capnometer. All patients received propofol anaesthesia and ventilation was adjusted according to clinical requirement. Arterial blood gas analyses were performed after induction, prior to dural incision, during surgery and before wound closure. Simultaneous haemodynamic and ventilatory parameters were also recorded. For 1007 paired measurements of PEco2 and Paco2 (mainstream, n = 503; sidestream, n = 504), the mean (SD) mainstream arterial to end-tidal carbon dioxide tension difference, 0.64 (0.16) kPa, was smaller than the corresponding sidestream values, 0.99 (0.40) kPa (p < 0.001). The limits of agreement for the mainstream analyser, 0.32-0.96 kPa, were also narrower than the sidestream recordings, 0.19-1.79 kPa (p < 0.001). In both capnometers, the arterial to end-tidal difference in carbon dioxide tension did not change with time. However, there was greater within-patient variation in the sidestream group. Our study showed that mainstream PEco2 provided a more accurate estimation of Paco2 than sidestream measurement.     

End-tidal carbon dioxide measurement and breathing system filters

Breathing system filters are recommended for use during general anaesthesia. Manufacturers of gas sampling equipment recommend that gas is sampled from the 'machine side' of these filters, thereby avoiding contamination of the sampling line and waterlogging in the case of heat and moisture exchangers. The aim of this study was to investigate differences between the measured end-tidal carbon dioxide values at either side of the filter. Fifteen adults were studied during mechanical ventilation and 15 during spontaneous ventilation under general anaesthesia. End-tidal carbon dioxide values were significantly lower at the machine side of the filter in both groups (p = 0.00001). The measurement error induced by the inclusion of the breathing system filter was significantly greater in the spontaneously breathing group (p = 0.0004).     

End-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation

In a porcine model of cardiac arrest, we investigated end-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation. After 15 minutes of cardiac arrest and after precordial compression and transthoracic countershocks had failed, extracorporeal circulation consistently restored spontaneous circulation. Native end-tidal carbon dioxide tension, which averaged 29.8 +/- 1.0 mm Hg before arrest, was only 5.2 +/- 0.8 mm Hg during precordial compression. After the start of extracorporeal circulation, native end-tidal carbon dioxide tension was measured during 15-second interruptions of pump flow. End-tidal carbon dioxide tension progressively increased with a corresponding increase in native cardiac index. The correlation coefficients between end-tidal carbon dioxide tension and native cardiac index averaged 0.92 +/- 0.03 (mean +/- standard error of the mean). When end-tidal carbon dioxide tension exceeded 15 mm Hg, mean aortic pressure in each instance was 60 mm Hg or greater, and the animal was successfully weaned from extracorporeal support. We conclude that end-tidal carbon dioxide tension serves as a reliable monitor of blood flow through the lung and therefore of native cardiac output during weaning from extracorporeal circulation. It therefore indicates when native cardiac output is likely to be adequate to sustain spontaneous circulation.     

End-tidal carbon dioxide during thoracotomy. Its relation to blood level in adults and children

The concentration of carbon dioxide in end-tidal gas was compared with the tension in arterial or superior vena caval blood during thoracotomy in twelve patients. In six adults requiring pulmonary resection, one-lung anaesthesia did not change the difference between the two measurements. In six children in whom a systemic to pulmonary arterial anastomosis was being created to improve pulmonary blood flow impaired by cyanotic congenital heart disease, occlusion of the pulmonary artery caused in increase in the blood-end-tidal carbon dioxide gradient. This change was particularly marked in two neonates and was of sufficient magnitude to render end-tidal monitoring unreliable in these circumstances.     

Do anxiety or hypocapnia predispose to apnoea after induction of anaesthesia?

We have studied the incidence of apnoea after induction of anaesthesia in patients allocated randomly to receive a standardized dose of either propofol or etomidate. We measured anxiety before operation with a standard questionnaire and end-tidal carbon dioxide concentration from a mask during breathing 35% oxygen, before induction of anaesthesia. Respiration was measured by pneumotachograph and impedance pneumograph. There was no significant relationship between anxiety score and end- tidal carbon dioxide concentration before operation. Patients given propofol (n = 26) received a median dose of 157 mg over 70 s, and 17 became apnoeic (median duration 24 s, quartile values 0, 76). Apnoea was more severe in patients whose preoperative end-tidal carbon dioxide value was less than the median value (median duration of apnoea 61 s compared with 10 s; P < 0.05). Patients given etomidate (n = 25) received 16.2 mg in 57 s, which was a significantly smaller fraction of the calculated dose requirement, and had significantly less apnoea: eight became apnoeic (median duration 0 s, quartile values 0, 23 s). There was no relationship between apnoea and end-tidal carbon dioxide concentration in these patients. Anxiety did not relate to the incidence of apnoea with either induction agent. We conclude that apnoea after induction of anaesthesia with propofol is more likely if hypocapnia is present but we could not relate apnoea or hypocapnia to anxiety in the ward before operation.      

Soda lime temperatures during low-flow sevoflurane anaesthesia and differences in dead-space

BACKGROUND: Sevoflurane degrades during low-flow anaesthesia to compound A, and high carbon dioxide absorbent temperatures cause increased degradation. The purpose of this investigation was to determine if larger tidal volumes, without increasing alveolar ventilation, decrease the temperature in the carbon dioxide absorber during low- and minimal-flow sevoflurane anaesthesia. METHODS: Prospective, randomized study, including 45 patients (ASA 1-2), scheduled for elective general or urology surgery. The patients were randomly assigned to one of three treatments. Patients in group 1 (NDS) received fresh gas flow of 1 litre/min without using additional dead-space volumes. In group 2 (DS + 1.0), the patients received fresh gas flow of 1 litre/min using additional dead-space volumes, placed between the Y-piece and the HME, and patients in group 3 (DS + 0.5) received the same technique with a fresh gas flow of 0.5 litre/min. The soda lime temperatures, dead-space volumes, end-tidal carbon dioxide, sevoflurane concentrations, ventilation volumes and pressures, absorbent weight and ear temperatures were measured. RESULTS: The maximum temperature of the soda lime was 44.1 +/- 1.1 degrees C in the NDS group, 37.8 +/- 0.8 degrees C in the DS + 1.0 group and 38.5 +/- 2.7 degrees C in the DS + 0.5 group (P<0.0001). The dead-space volume between the Y-piece the tracheal tube was 164 +/- 69 ml in the DS + 1.0 group and 196 +/- 15 ml in the DS + 0.5 group (P<0.05). The ventilator pressure were higher in the DS groups compared with the NDS group (P<0.001). Soda lime weight increased in all groups. End-tidal carbon dioxide, sevoflurane concentrations and ear temperatures were similar between the groups. CONCLUSION: Increasing dead-space volumes can reduce carbon dioxide absorber temperature during low- and minimal-flow sevoflurane anaesthesia.     

A non-rebreathing coaxial anaesthesia system: dependence of end-tidal gas concentrations on fresh gas flow and tidal volume

A non-rebreathing adaptation of the Bain coaxial anaesthesia circuit was developed in Nepal as a simple and economical anaesthetic system for underdeveloped countries. It was made by inserting a coaxial (Bain) tubing between an Ambu-E valve and an Ambu self-inflating bag. The present study examined the dependence of end-tidal gas concentrations on fresh gas flow and tidal volume during halothane/oxygen/air inhalation anaesthesia. Four levels of fresh gas flow with normocapnia (0.2–3 l.min⁻¹) and three levels of tidal volume at a constant respiratory rate of 15 breath.min⁻¹ (to achieve end-tidal carbon dioxide values of 4 ± 0.5%, 5 ± 0.5% and 6 ± 0.5%) were introduced in random order. Twelve ASA class 1 and 2 adult patients having intra-abdominal or pelvic surgery were studied. With increasing fresh gas flow rates, there were proportionate increases in the end-tidal concentrations of oxygen and halothane; with decreasing tidal volume and therefore less air dilution, there were proportionate increases in the end-tidal concentrations of carbon dioxide, oxygen and halothane. Both effects were statistically and clinically significant. Thus, when this system is used as described, the end-tidal concentrations of oxygen and halothane are highly dependent upon both the fresh gas flow and the tidal volume.     

An evaluation of capnography monitoring during the apnoea test in brain-dead patients

BACKGROUND AND OBJECTIVE: Diagnosis of brain death usually requires the absence of spontaneous respiratory movements during the apnoea test and an arterial carbon dioxide partial pressure above 60 mmHg. On the other hand, although capnography (end-tidal CO(2)) is currently monitored in intensive care unit patients, it has not been evaluated during the apnoea test in brain-dead patients. Therefore, the aim of this prospective study was first to investigate the usefulness of capnography monitoring, and secondly to evaluate the variation of the carbon dioxide partial pressure-end-tidal CO(2) gradient during the apnoea test in clinically brain-dead patients. METHODS: After local Ethics Committee approval, 60 clinically brain-dead patients were investigated. End-tidal CO(2) was continuously recorded before, during and after the apnoea test. Arterial blood gases were sampled immediately before and after the apnoea test for calculation of the carbon dioxide partial pressure-end-tidal CO(2) gradient. RESULTS: The apnoea test was clinically positive in 58 patients, whereas end-tidal CO(2) was equal to 0 during the apnoea. During the 20-min apnoea test, carbon dioxide partial pressure increased from 40 +/- 7 to 97 +/- 19 mmHg (P < 0.001) with a rate of 2.8 +/- 0.9 mmHg min(-1), end-tidal CO(2) increased from 31 +/- 6 to 68 +/- 17 mmHg (P < 0.001) and carbon dioxide partial pressure-end-tidal CO(2) gradient increased from 9 +/- 4 to 29 +/- 10 mmHg (P < 0.001). In two patients, the apnoea test was clinically negative because of the occurrence of spontaneous respiratory movements, whereas capnography showed contemporaneously significant increases in end-tidal CO(2). CONCLUSIONS: End-tidal CO(2) should be systematically monitored and recorded, at least for medico-legal considerations, during the apnoea test in brain-dead patients. The high variability in the carbon dioxide partial pressure-end-tidal CO(2) gradient increase precludes any extrapolation of the carbon dioxide partial pressure from the end-tidal CO(2) at the end of the apnoea test.     

Arterial to end-tidal carbon dioxide tension difference in anaesthetized adults mechanically ventilated via a laryngeal mask or a cuffed oropharyngeal airway.

To evaluate arterial (PaCO2), end-tidal (PETCO2) and carbon dioxide tension difference during mechanical ventilation with extratracheal airways, 60 patients ASA physical status I-II, receiving general anaesthesia for minor extra-abdominal procedures were randomly allocated to receive either a cuffed oropharyngeal airway (group COPA, n = 30) or a laryngeal mask (group LMA, n = 30). The lungs were mechanically ventilated by IPPV using a 60% nitrous oxide and 1-1.5% isoflurane in oxygen mixture (VT = 8 mL kg-1; RR = 12 b min-1; l/E = 1/2). After PETCO2 had been stable for at least 10 min after airway placement, haemodynamic variables and PETCO2 were recorded and an arterial blood sample was obtained for measurement of PaCO2. No differences in anthropometric parameters, smoking habit, haemodynamic variables and incidence of untoward events were observed between the two groups. Airway manipulation, to maintain adequate ventilation, was required in only nine patients in the cuffed oropharyngeal airway group (30%) (P < 0.0005); however, in no case was it necessary to remove the designated extratracheal airway due to unsuccessful mechanical ventilation. The mean difference between arterial and end-tidal carbon dioxide partial pressure was 0.4 +/- 0.3 KPa in the laryngeal mask group (95% confidence intervals: 0.3-0.5 KPa) and 0.3 +/- 0.26 KPa in the cuffed oropharyngeal airway group (95% confidence intervals: 0.24-0.4 KPa) (P = NS). We conclude that in healthy adults who are mechanically ventilated via the cuffed oropharyngeal airway, the end-tidal carbon dioxide determination is as accurate an indicator of PaCO2 as that measured via the laryngeal mask, allowing capnometry to be reliably used to evaluate the adequacy of ventilation.     

The influence of alfentanil pre-treatment on ventilatory effects of doxapram following induction of anaesthesia with propofol

Background : Hypoventilation may occur following induction of anaesthesia with propofol and is potentiated by concurrent use of opioid drugs. This effect is undesirable in patients who will continue to maintain spontaneous respiration during anaesthesia and surgery. The analeptic drug doxapram is known to have selective respiratory stimulatory effects but its action during induction of anaesthesia has been inconsistent.
Method : In a double-blind, placebo-controlled study, the influence of alfentanil pre-treatment on the ventilatory effects of doxapram given during induction of anaesthesia with propofol was studied in 40 patients. Four groups of ten patients (two groups pre-treated with 7 μg·kg^-1 of alfentanil and two groups with saline) were randomly allocated to receive either 0.5 mg·kg^-1doxapram or saline following infusion of propofol to loss of verbal contact.
Results : In the groups that received doxapram, minute volumes were significantly increased and end-tidal carbon dioxide concentrations were significantly reduced compared to control groups, although the duration and extent of these effects were less in the group that received alfentanil. Doxapram also reversed an alfentanil-induced reduction in respiratory rate. No adverse cardiovascular or neurological stimulatory effects of doxapram were evident at any time.
Conclusion : We conclude that doxapram 0.5 mg·kg^-1 is effective in augmenting ventilation that has been obtunded following induction of anaesthesia with propofol in patients pre-treated with alfentanil.