Predicted normocapnea in infants and children using the Bain circuit with controlled ventilation

We have constructed a nomogram for fresh gas flow (VFG) and minute ventilation (VE) for paediatric anaesthesia during controlled ventilation using the Bain coaxial Mapleson D circuit. VFG was based upon the assumption of a high fresh gas utilization because of a low VFG/VE ratio (0.67) and known figures of carbon dioxide elimination. The formulas VFG = 27.8 x VCO2 and VE = 1.5 x VFG were used to calculate the necessary flows to generate normocapnea. The nomogram was evaluated in 59 children (6-62 kg, age 5 months-14 years). PaCO2 (mean +/- s.d.) was 5.0 +/- 0.5 kPa (38 +/- 4 mmHg) with a total range of 3.9-6.3 kPa (29-47 mmHg). Ninety percent of the children had a PaCO2 of 5.7 kPa (43 mmHg) or lower. There was no correlation between body weight and PaCO2. Hence, there was no difference in mean values between children below or above a body weight of 20 kg.     

Intra-arterial and extra-arterial pH, PCO2 and PO2 monitors

In vitro blood gas analysers inherently limit the frequency of serial blood gas measurements because of blood loss and cost. In vivo blood gas monitors eliminate an inherent cost and blood loss associated with measurement. Optode microsensing is a technology that can be readily adapted to in vivo measurement of pH, PCO₂ and PO₂. Optode-based intra-arterial devices that display continuous values have been developed that are practical for routine use but consistent performance remains a problem; an extra-arterial device that provides intermittent values has been shown to be consistent but is not yet available for routine use. The transfer of blood gas measurements from laboratory analysers to the combination of point-of-care analysers and monitors should have as profound an impact on acute respiratory care as did the introduction of laboratory-based blood gas analysers over 30 years ago. However, we must be sure these devices are reliable, consistent and cost beneficial in order to avoid widespread adoption of yet another technology that provides more data, more cost, and questionable patient benefit.     

Changes in the arterial to end-tidal Pco2 differences during coronary artery bypass grafting

The arterial to end-tidal PCO2 difference, PaCO2-PE,CO2, was measured at four different stages during coronary artery bypass grafting in 43 patients: 1) before sternotomy; 2) after sternotomy, sternum retracted; 3) after bypass, sternum still retracted; 4) sternum closed. Mean PaCO2-PE,CO2 initially was 0.6 kPa and changed scarcely at all during the procedure. There were, however, some moderate individual changes in PaCO2-PE,CO2 during surgery, the range of changes compared to the initial value being from -1.4 to +1.3 kPa. The standard deviations for the changes from stage to stage were 0.3-0.4 kPa. PaCO2-PE,CO2 changed by more than 0.5 kPa on only 12 occasions in ten patients. The limitations of PaCO2-PE,CO2 as an index of the alveolar deadspace fraction and the efficiency of ventilation are discussed.     

End-tidal CO2 monitoring

Two cases of malignant hyperthermia are described where the earliest sign was a rise in the end-tidal CO2 concentration. This led to nearly immediate detection and adequate treatment with sodium dantrolene. These cases demonstrate the efficacy of monitoring end-expired CO2 concentrations in patients at risk from malignant hyperthermia, as well as a means for following the adequacy of treatment.     

Reliability of CO2 measurements from the airway by a pharyngeal catheter in unintubated, spontaneously breathing subjects

Although several short communications have appeared describing attempts to record the concentrations of carbon dioxide (CO₂) from the unintubated airway by a catheter placed in the nose, so far only few reports have documented the reliability of the method. To evaluate the reliability of CO₂ measurements by a catheter in the open, unintubated airway during spontaneous respiration, a 12 CH PVC catheter was forwarded through the nostril to the hypopharynx and connected to a capnograph in nine healthy volunteers. Another capnograph was connected to a tightly fitting face mask and simultaneous CO₂ recordings were attained from the two parts of the airway during normoventilation, hyperventilation and rebreathing. A corresponding blood sample was drawn from the radial artery for blood gas analysis. The configurations of the capnograms recorded from the pharyngeal catheter were similar to those recorded from the face mask. The results were analysed by a multifactor analysis of variance. The carbon dioxide tension ( p CO₂) was significantly influenced by degree of ventilation ( P <0.0001), subject ( P <0.0001), measurement site ( P =0.030) and interaction subject-ventilation ( P =0.015). In spite of the significant influence of the measurement site, the difference between end tidal carbon dioxide tension ( P CO₂(ET)) and carbon dioxide tension in arterial blood ( P CO₂(a)) was small. The mean differences between paired measurements ( p CO₂(ET)- p CO₂(a)) were -0.10 kPa±0.41 kPa (mean±SD) for the catheter and -0.20 kPa ±0.43 kPa for the face mask. The study demonstrates that reliable recordings of CO₂ concentrations during spontaneous respiration can be obtained by a thin catheter positioned in the hypopharynx.     

PCO2 electrodes at the surface of the kidney detect ischaemia

Background: Under ischaemic (anaerobic) conditions there will be an accumulation of CO₂ in the tissue secondary to a build up of protons that is buffered by HCO₃^-. We reasoned that CO₂ could be measured at the surface of the kidney by PCO₂ electrodes to detect ischaemic conditions. Methods: Anaesthetized, mechanically ventilated pigs (25–30 kg) were investigated. Two acute porcine models, one of haemorrhagic shock and one of renal artery stenosis were used. Renal blood flow was gradually decreased, either by successive episodes of bleeding through the arterial cannula or by successive snaring of the renal artery. Results: In both models we found that with decreased blood flow but maintained aerobic metabolism (supply independence) PCO₂ both at the surface of the kidney and in the renal vein increased by 2–3 kPa. Thus, the tissue-venous PCO₂ difference did not change much. At DO_2crit, i.e., at the transition to supply-dependent O₂ consumption, the tissue PCO₂ started to increase rapidly, as did the tissue-venous PCO₂ difference. This is compatible with the notion that a hallmark of ischaemia is decreased ability of the blood to transport away waste products because the contact between large parts of tissue and blood is virtually non-existent. In the renal artery stenosis model kidney surface PCO₂ values rose from a baseline of 6.6±0.6 kPa (mean±SEM) to a value near DO_2crit of 10.6±0.8 kPa, reaching a final value of 29.9±3.5 kPa at no flow. PCO₂ in the renal vein, however, reached a maximum of only 8.2±0.6 kPa. Numbers very similar to these were also found in the haemorrhagic model. The urine production decreased before the onset of ischaemia. When surface PCO₂ values increased sharply indicating ischaemia, the urine production was zero. Lactate production by the kidney correlated very well with increasing tissue PCO₂ values further corroborating that anaerobic metabolism was detected with the electrodes. Conclusion: We conclude that PCO₂ electrodes placed at the surface of the kidney detect renal cortical ischaemia.     

Measurement of transcutaneous P±o2, Pco2 and skin blood flow at different probe temperatures using mass spectrometry

Transcutaneously measured partial pressures of oxygen and carbon dioxide (PtcO2, PtcCO2) approximate the corresponding arterial values at a probe temperature of 44 degrees C. The temperature-dependent increase of PtcO2 and PtcCO2 is caused by an increased skin perfusion, a decrease in the mean diffusion path, a change of skin metabolism, a decrease of tissue solubility of oxygen and carbon dioxide and a right shift of the oxygen and carbon dioxide binding curves of blood. Seven healthy volunteer test subjects participated in the study. A transcutaneous probe connected to a mass spectrometer was placed on the earlobe of the test subject. Four measurements of the transcutaneous PO2, PCO2 and skin blood flow (from the washout kinetics of argon) were determined on each test subject. The first measurement was made with a transcutaneous probe temperature of 37 degrees C. The probe temperature was then increased to 44 degrees C before the next determination. Finally, two determinations were made at 37 degrees C, separated by a time interval of 1 h. The PtcO2 and skin blood flow increased when the probe temperature increased from 37 degrees C to 44 degrees C. However, when the probe temperature was decreased again from 44 degrees C to 37 degrees C, the estimated skin blood flow returned to the initial value while the PtcO2 remained unchanged. It required a further 1 h before the PtcO2 returned to the initial value at 37 degrees C. The most likely explanation of the experimental results is that heating of the skin to 44 degrees C causes a reversible decrease in the skin metabolism.     

Brain tissue PO2, PCO2, and pH during cerebral vasospasm

BACKGROUND

The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients.

METHODS

After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. Brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies.

RESULTS

Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO₂) remained above 20 mmHg, carbon dioxide pressure (PCO₂) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO₂ was not different from the control group. However, PCO₂ increased to 60 mmHg and pH decreased to 6.7 (p < 0.001).

CONCLUSION

In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO₂ compared to controls. However, there was no significant change in PO₂ levels associated with vasospasm. Brain tissue monitoring can provide an indication of ischemia during vasospasm.     

Effects of esmolol on haemodynamic response to CO2 pneumoperitoneum for laparoscopic surgery

Background : Carbon dioxide (CO₂) pneumoperitoneum for laparoscopic surgery increases arterial pressures, systemic vascular resistance and heart rate and decreases urine output.
Methods : In this double-blind randomized study esmolol, an ultrashort-acting β1-adrenoceptor antagonist was compared with physiological saline (control) in 28 patients undergoing laparoscopic surgery in standardized 1 MAC isoflurane anaesthesia. Alfentanil infusion was used to prevent the increase of mean arterial pressure more than 25% from baseline.
Results : Esmolol effectively prevented the pressor response to induction and maintenance of CO₂ pneumoperitoneum. Significantly ( P <0.001) less alfentanil was needed in the esmolol group than in the control group. Urine output was higher ( P <0.05) and plasma renin activity ( P <0.01) and urine N-acetyl-β-D-glucosaminidase levels lower in the esmolol group when compared with the control group.
Conclusions : Esmolol blunts the pressor response to induction and maintenance of pneumoperitoneum and may protect against renal ischaemia during pneumoperitoneum.     

Gas exchange during thoracotomy in children. A study using the single-breath test for CO2

Gas exchange during thoracotomy was studied in 13 children aged 6 months to 14 years (median age 5 years), anaesthetized for repair of coarctation of the aorta or closure of a patent ductus arteriosus. All received halothane in equal parts of N2O/O2 supplemented with fentanyl. CO2 single-breath tests were obtained with a computerised on-line system based on the Servo ventilator. From signals for airway flow pressure, CO2 concentration and timing, the computer calculated the airway deadspace (VDaw) and the static compliance and resistance of the respiratory system. Given a value for PaCO2, the computer also calculated the physiological and alveolar deadspaces. Measurements were taken at six stages during the procedure, starting with the supine position before surgery. After turning to the lateral position, airway deadspace increased by 19%, thus increasing the physiological deadspace fraction. When the pleura was opened, both VDaw and PaO2 were reduced. When the upper lung was retracted, compliance was reduced and also PaO2 - the minimum value noted was 17.3 kPa. Hypoxic PaO2 values were possibly avoided because both ventilation and perfusion were reduced in the retracted lung. The alveolar deadspace fraction increased during these intra-operative stages. Although the net effect of the changes in airway and alveolar deadspace during surgery was a significant increase in physiological deadspace fraction (from 0.23 to 0.28), gas exchange could be maintained at the cost of only moderate increases in peak airway pressure: the mean increase was from 2.4 to 2.8 kPa (24 to 29 cmH2O).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary blood flow reduction by prostaglandin F2α and pulmonary artery balloon manipulation during one-lung ventilation in dogs

The purpose of this experimental study was to compare two methods of pulmonary blood flow manipulation during one-lung ventilation (OLV), either reducing pulmonary blood flow to the non-ventilated lung by inflation of a pulmonary artery catheter balloon (PAB) or by infusion of prostaglandin F2 alpha (PGF2 alpha). Seven anaesthetized dogs were intubated with a Kottmeier endobronchial tube and ventilated with 66% O2. Systemic and pulmonary pressures and blood gases, cardiac output and airway pressure were measured, and the venous admixture (QSP/QT) was calculated. During two-lung ventilation (TLV) Pao2 was 43.6 +/- 1.9 kPa (mean +/- s.d.) and (QSP/QT) was 11 +/- 3%. OLV reduced Pao2 to 12.1 +/- 1.6 kPa (P less than or equal to 0.001) and increased QSP/QT to 40 +/- 4% (P less than or equal to 0.001). Mean pulmonary artery pressure and airway pressure increased. PAB inflation caused an increase in Pao2 to 19.9 +/- 2.9 kPa (P less than or equal to 0.02) and a decrease in QSP/QT to 27 +/- 6% (P less than or equal to 0.001). PGF2 alpha infusion (1.2 micrograms kg-1 min-1) into the pulmonary artery of the non-ventilated lung increased Pao2 to 22.4 +/- 3.3 kPa (P less than or equal to 0.001) and decreased QSP/QT to 25 +/- 4 (P less than or equal to 0.001). PGF2 alpha infusion resulted in a small increase in mean systemic and pulmonary artery pressures. During the infusion of 1.2 micrograms kg-1 min-1 of PGF2 alpha no signs of bronchoconstriction were observed. PAB inflation and PGF2 alpha infusion were equally effective in improving oxygenation and reducing venous admixture during OLV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intermittent high frequency ventilation: a new mode to measure changes in lung volume and alveolar gas concentration, enhance CO2 elimination and reduce intrapulmonary pressures

A new method of artificial ventilation, intermittent high frequency ventilation (IHFV), is described in which high frequency ventilation (HFV) is intermittently interrupted so that short periods of ventilation and pauses in ventilation occur in sequence several times a minute. During the pauses in ventilation the increase in lung volume, which occurs during the short periods of HFV, is either exhaled completely or to a predetermined level which prevents sustained hyperinflation of the lungs but allows the maintenance of PEEP if required. The volume of gas expired during the ventilation pauses, i.e. gas retained during the periods of HFV, is measured. When this trapped gas is exhaled completely, the mean airway and compliance pressures are reduced by up to 50% compared to continuous HFV at the same frequency, inspiration:expiration (I:E) ratio and low tidal volume (VT). The alveolar CO2 concentration was measured in gas expired towards the end of the pauses in ventilation. CO2 elimination was improved, especially at high frequencies of ventilation, which allowed a further reduction in inflation pressures while maintaining a constant PaCO2.     

Pulmonary ventilation, CO2 response and inspiratory drive in spontaneously breathing young infants during halothane anaesthesia

Pulmonary ventilation, CO2 response and inspiratory drive were studied during halothane anaesthesia prior to surgery in 13 spontaneously breathing infants less than 6 months of age. Pneumotachography and capnography were used. Airway and oesophageal pressures were measured and occlusion tests were performed at functional residual capacity. Measurements were made before and during 8 min of 4% CO2 stimulation. Inspiratory drive increased significantly (P less than 0.001) at CO2 stimulation. This resulted in increased minute ventilation (P less than 0.001) and tidal volume (P less than 0.001) while respiratory rate was unchanged. As VBohrD/VT ratios were the same, the net effect was increased alveolar ventilation (P less than 0.001). CO2 elimination was unpredictable in these young infants and decreased during CO2 stimulation (P less than 0.05), while mean end-tidal CO2 concentration only increased from 5.2 to 6.3% (P less than 0.001). The ventilatory response to 4% CO2 could therefore be deemed to be adequate during the short period (8 min) of CO2 breathing. However, this was achieved at the cost of increased work as witnessed by the increased ratio between minute ventilation and CO2 elimination (P less than 0.01). Stabilisation of end-tidal CO2 concentrations during CO2 inhalation took only 10 s while the maximal increase in ventilation volumes was not achieved until after 150 s. It is concluded that young spontaneously breathing infants anaesthetized with halothane (MAC 1.3) have an increased respiratory drive with greater tidal volumes during CO2 stimulations. Respiratory timing, dynamic compliance and total pulmonary resistance were, however, uninfluenced by 4% CO2 stimulation. Increased monitoring of CO2 output in anaesthetized infants is suggested.     

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.     

Fresh gas flow changes during controlled mechanical ventilation with the circle breathing system have significantly greater effects on the ventilatory parameters of toddlers compared with children*

Fresh gas flow into a circle system can affect the delivered minute ventilation because fresh gas flow augments the flow delivered by the ventilator bellows during inspiration. After establishing a stable ventilatory pattern with 3.0 l·min^-1 fresh gas flow into a circle system, changes in peak inflation pressure, minute ventilation and end-tidal carbon dioxide were measured at 1.5 l·min^-1 and 6.0 l·min^-1 in 10 toddlers (10–20 kg) and 10 children (30–60 kg). Changes in all variables were observed but these changes were greater in toddlers compared with children (P < 0.001). Some toddlers were noted to have as much as a 37% change in ventilatory parameters when fresh gas flow was altered between 1.5 and 6.0 l·min^-1. Whenever changes are made in fresh gas flow, compensatory changes in minute ventilation should be considered to avoid unintended hyperventilation or hypoventilation. This is especially important during anaesthesia for toddlers.     

A New Perfusion Circuit for the Newborn with Lung Immaturity: Extracorporeal CO2 Removal via an Umbilical Arteriovenous Shunt During Apneic O2 Diffusion

In spite of improved prophylaxis and therapy, the respiratory distress syndrome is still a major cause of morbidity and mortality in premature babies. Owing to the fact that a number of patients are unresponsive to other methods of neonatal care, an increasing number of perinatal centers have started to treat this group of patients with extracorporeal membrane oxygenation successfully. To make the extracorporeal gas exchange more practicable for the neonate directly after birth, a modification of this method using an umbilical arteriovenous shunt for CO2 removal in apneic premature lambs as an animal model was evaluated. A miniaturized low-resistance extracorporeal circuit that is totally incorporated in a regular intensive care baby incubator was developed. The benefit of using extracorporeal CO2 removal in very low birth weight newborns could be a conditioning of the premature lung during a short period of bypass, after which ventilation at nontraumatic pressures and nontoxic O2 concentrations would become possible.