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Measurements of arterial carbon dioxide tensions (PaCO2) were made in children between nine months and twelve years of age, using a modification of the rebreathing technique of Campbell and Howell, during anaesthesia with halothane, nitrous oxide and oxygen, maintaining spontaneous respiration. The accuracy of this method was investigated by a series of double readings, in which the rebreathing times were varied, and by comparison with samples of arterial blood analyzed by the Astrup technique. The results of these experiments showed this basically simple method to be adequate for measuring PaCO2 in clinical anaesthesia.

The relative benefits and hazards of bronchial lavage with 10% acetylcysteine (Mucomyst) compared to sodium chloride solution was studied in 14 patients with cystic fibrosis who were treated on 16 occasions. Lavage with acetylcysteine produced a significant increase in arterial carbon dioxide tension (Paco 2 ) and a decrease in arterial oxygen tension (Pao 2 ) immediately after lavage. Lavage with sodium chloride solution produced a decrease in Paco and an increase in `Pao 2 . Regardless of lavage agent, pulmonary function was impaired for 48 to 72 hours after lavage, and three patients developed pneumonia within three days after lavage. When bronchial lavage was used as one part of a complete therapeutic program, some improvement in pulmonary function could be demonstrated two to six weeks after therapy.

Cerebral vasoreactivity to CO(2), calculated by linear regression of total cerebral hemoglobin, measured by near infrared spectroscopy, and corresponding PaCO(2), in infants

The CBF was measured on the first three days of life in 22 mechanically ventilated, preterm neonates (mean gestational age 29.5 weeks) with simultaneous recordings of arterial carbon dioxide tension (PaCO2), arterial oxygen tension (PaO2), haemoglobin concentration (Hgb), haemoglobin oxygen saturation and mean arterial blood pressure (MABP). CBF infinity tended to increase slightly with age. The intra-individual variation of CBF infinity was positively related to changes in PaCO2 (p = 0.0004) and inversely related to changes in Hgb (p = 0.029). Neither PaO2 nor MABP achieved a significant relation to changes in CBF infinity. Thus, the mean CBF infinity -CO2 reactivity was calculated to 22.1% per kPa whereas CBF infinity increased by a mean of 11.9% per mM decrease of Hgb thereby providing a constant oxygen delivery to the brain. It is concluded that PaCO2 and Hgb have the expected effect on CBF infinity in preterm neonates even during respiratory distress shortly after birth.

Summary Arterial blood gases were analysed before and approximately one hour after premedication in two groups of 10 patients awaiting cardiac surgery. One group received intramuscular papaveretum and hyoscine, the other papaveretum and glycopyrronium. Similar, small but statistically significant reductions in mean arterial oxygen tension and oxygen saturation, and increases of arterial carbon dioxide tension occurred in both groups. Hypoxaemia in individual patients was unpredictable and in some was clinically relevant.

Summaries of papers delivered at the meeting are printed below. A selection of these papers will be printed in full in this and subsequent issues.

Hospital records of 91 consecutive near-drowning victims were studied retrospectively. Eighty-one (89 percent) of these patients survived. Patients who were alert on arrival at the emergency room survived, but those who were comatose and had fixed dilated pupils died. Other states of consciousness were unreliable predictors of survival. All patients with a normal chest roentgenogram on admission survived; however, values for arterial oxygen tension (PaO2) did not necessarily correlate with the chest roentgenograms. Values for arterial blood gas tensions and pH varied widely, as follows: PaO2, 25 to 465 mm Hg; arterial carbon dioxide tension (PaCO2), 17 to 100 mm Hg; pH, 6.77 to 7.50; and arterial bicarbonate level, 6.6 to 29.7 mEq/L. The ratio of PaO2 to the fractional concentration of oxygen in the inspired gas (FIo2), which was calculated to standardize PaO2 data for varying concentrations of inspired oxygen, ranged from 30 to 585 mm Hg. Only one patient with a ratio of PaO2/FIo2 greater than 150 mm Hg on admission subsequently died; this was a neurologic rather than a pulmonary death. Serum electrolytic concentrations and values for hemoglobin level and hematocrit reading neither predicted survival nor indicated that a threat to life existed. Steroid and prophylactic antibiotic therapy did not appear to increase the chance of survival. Observations on these patients are discussed in light of previous experiments in animals, and an approach to therapy is suggested.

The relationship between end-tidal carbon dioxide tension(PECO2) as measured by infrared analysis(Datascope Accucap, U.S.A.) and arterial carbon dioxide tension(PaCO2) during general anesthesia was systemically examined in fifty relatively healthy patients(ASA class 1). Body temperature was measured to determine the variation in PaCO2 minus PECO2. The results were as follows: 1) The mean PEzCO2 was 26.2±0.7 torr. 2) The mean PaCO2 was 31.6±0.8 torr. 3) The average of PaCO2 minus PECO2 was 5.1±0.6 torr. 4) PaCO2 was directly related to PECO2. An equation was obtained by simple regression analysis to predict PaCO2. PaCO2=0.899. PECO2+7.57(r=0.715; P

Responses of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2) were studied by near infrared spectroscopy during the first week of life in 12 newborn infants, 11 of whom were receiving mechanical ventilation. 5 of the infants were thought to have normal brains, and 7 had various forms of cerebral injury. In the normal infants, increases in PaCO2 of about 1-2kPa caused cerebral blood volume to increase by 0.5 to 1.8ml.100g−1.kPa−1: the size of the increase appeared to be gestation-dependent. Estimated cerebral blood flow increased correspondingly. In the 7 infants with cerebral injuries the responses to changes in PaCO2 were usually less. In 3 term infants who had been severely birth-asphyxiated they were absent or grossly reduced and all 3 had elevated cerebral blood volumes. 3 of the 7 infants died and all 4 survivors had loss of brain tissue. We conclude that: 1) the sensitivity of the cerebral vasculature to PaCO2 probably increases with gestation, 2) cerebral injury is associated with diminished or absent responses to PaCO2.

Measurement of arterial carbon dioxide tension (paCO2) is an invasive technique for determining the adequacy of ventilation and, therefore, is associated with possible morbidity. Consequently, a non-invasive means for estimating paCO2 is desirable. A Chemetron mass spectrometer (MS) with a response time of 0.68 sec to 63% of a step change in CO2 and analytic accuracy for CO2 of ± 2% was used to measure PECO2 of neonates on IPPV/CPAP. Gas was continually sampled from 1.0 cm beyond the plastic adapter of an oral ET tube via a catheter with inner diameter 0.38 mm. 9 neonates (mean BW 2182g, range 870-3440; mean GA 33.8 wk, range 26-40) with cardiopulmonary diseases (5 HMD, 2 aspiration, 1 each PDA, CHD, BPD, pneumothorax) were studied at an initial mean age of 82 hrs (6/9 < 72 hrs), 75 paired comparisons of PECO2 and paCO2 had a correlation of 0.69 (p < 0.001) and a mean gradient (paCO2-PECO2) of 8.3 torr (range +23 to -3). 61.3% of the gradients were ≤ 10 torr. We conclude that the MS is a useful monitoring device but that the correlation between paCO2 and PECO2 was adversely affected by the relatively long response time of the total system. We speculate that reduction of this parameter would enhance the usefulness of the MS by increasing the correlation and decreasing the gradient.

Previous studies in adults have shown that CO2 is a major factor in cerebral blood flow regulation. The present study investigates the effect of hyperventilation on cerebral and other organs blood flow in 8 newborn lambs 15 days old. Following chronic catheterization,blood gases, Hct, Hb, pH, lactates, pyruvates, and regional blood flows using the microsphere technique were obtained prior to and following hyperventilation. Mean values for blood flow ± SD in ml/min/100g tissue at a baseline PaCO2 of 36 mmHg and after hyperventilation to 20 and 12 mmHg respectively were: brain - from 118 ± 14 to 83 ± 10 to 59 ± 17 (p < 0.05); adrenal - from 418 ± 60 to 365 ± 45 to 303 ± 40 (p < 0.05); kidney - from 458 ± 49 to 408 ± 31 (p < 0.05) to 201 ± 42 (p < 0.01); heart - from 111 ± 32 to 88 ± 21 to 59 ± 15 (NS). Cardiac output did not significantly change from a mean value ± SD in ml/min/kg of 197 ± 39 to 161 ± 33 to 108 ± 24 at 20 and 12 mmHg respectively. There was no change in whole blood buffer base with acute changes in PaCO2. This data demonstrates that hyperventilation reduced organ blood flow independent of cardiac output. Cerebral blood flow in the newborn lambs as in the adults seems sensitive to changes in PaCO2 with the reduction being most marked (50% from baseline value) at a PaCO2 of 12 mmHg. These data also suggest that a similar mechanism may be responsible for the reduction in renal and adrenal blood flows.

The transcutaneous technique of measuring carbon dioxide tension (tcPCO2) was studied in 30 adult neurosurgery patients undergoing nitrous oxide-enflurane or nitrous oxide-fentanyl anesthesia to determine the relationship between tcPCO2 and PaCO2. tcPCO2 was an accurate (r = 0.9) and clinically useful trend indicator of PaCO2. The ability to detect trends was unaffected by the type of anesthetic agent used. The technique was less useful in predicting absolute values for PaCO2 (r = 0.64). This technique may be particularly useful in situations in which control PaCO2 is essential to patient management.

Cardiovascular and pulmonary effects following the administration of 0.3 mg/kg of etomidate were studied in patients with documented cardiac disease. The only significant change was a slight elevation (2 torr) in arterial carbon dioxide tension.

A 51-year-old woman with chronic respiratory failure (status after tuberculosis) was given an infusion of doxapram hydrochloride (1 to 2 mg/kg of body weight per hour) for four episodes of acute exacerbation of her condition. Treatment with the drug prevented worsening of hypercapnia in the four episodes, when administration of 24 percent oxygen had occasioned rises in the arterial carbon dioxide tension of 23, 10, 9, and 7 mm Hg.

SUMMARY Dynamic compliance, resistance to gas flow and respiratory work were determined in 20 patients during anaesthesia and controlled ventilation with the Engstrom respirator. The compliance was measured continuously with the aid of a “respiration analyser” and a pneumotacho-calibrator, which allows breath-by-breath registration and automatic calibration of gas flow, compliance and respiratory work without the interruption of the patient's ventilation. Ventilatory frequencies utilized (18-20/min.) and tidal volume were unchanged during the periods of investigation, which were of an average duration of 233 minutes (range 60-570 minutes). Compliance at the beginning of the controlled ventilation was 44.5±2.7 ml/cm H2O and at the end 44.8 ±2.2 ml/cm H2O. A sustained or forced inflation for 20-40 seconds did not result in any significant changes in compliance. The resistance to gas flow was measured at 0.5 L/sec. and at maximum flows (approx. 0.8-1.2 L/sec.) and was 13.3±1.0 cm H2O/L/sec. and 14.4±1.0 cm H2O/L/sec, respectively. The resistance to the endotracheal tubes and connections corresponded to 7-8 cm H2O/L/sec. The inspiratory work of breathing varied between 0.55 and 1.31 kpm/min. with an estimated proportion of 4:1 between elastic and resistive work. The ventilatory volumes used resulted in arterial carbon dioxide tension values close to 40 mm Hg, indicating the rationale of calculating ventilatory volumes from a special nomogram. Alveolar-arterial oxygen tension differences were within normal ranges (80 ±14 mm Hg, range 28-143 mm Hg). There was no fall in arterial oxygen tension during die period of controlled ventilation, and forced inflations did not improve the arterial oxygen tensions. It is believed that the special flow-pressure pattern of die Engstrom respiratoran accelerating gas flow with a variable end-inspiratory pressure plateaucounteracts any tendency to alveolar collapse and possible decrease in compliance. This assumption gains strength from experimental studies in which the difference in the distribution of insufflated volumes and changes in apparent compliance have been analysed for constant and accelerating gas flows. The variable end-inspiratory pressure plateau of the Engstrom respirator offers breadi-to-breath “mini-sighs,” and there is thus no need to provide this machine with any special device for “deep” sighs, as has recently been suggested. Our findings indicate that there is an explanation of why others have found a decrease in compliance during controlled ventilation in contrast to our results. This is probably due to the utilization of constant gas flows and the absence of an end-inspiratory plateau, which will have an unfavourable effect on the pulmonary mechanics. ZUSAMMENFASSUNG Die dynamische Compliance, der Gasstromwiderstand und die Atemarbeit wurden bei 20 Patienten wahrend der Narkose unter kunsdicher Bcat-mung mit dem Engstrom-Respirator bestimmt. Die Compliance wurde kontinuierlich mit Hilfe eines «respiration analyzer» und eines Pneumotacho-kalibrators gemessen, wobei Atemzug fur Atemzug-Registrierung und auto-matische Kalibrierung des Gasstromes, der Compliance und der Atemarbeit moglich war, ohne die Beatmung des Patienten unterbrechen zu mussen. Die Atemfrequenzen (18-20/min) und Atemvolumina blieben wahrend der Unter-suchungsperioden, die zwischen 60 und 570 Minuten, im Mittel 230 Minuten, bctrugen, unverandert. Zu Beginn der kontrollierten Beatmung war die Compliance 44,5±2,7 ml/cm H2O und am Ende 44,8 ± 2,2 ml/cm H2O. Forcierte Uberblahung wahrend 20-40 sec fuhrte zu keinen signifikanten Anderungen der Compliance. Der Gasstromwiderstand wurde bei 0,5 1/sec und bei Maximal-stromung von 0,8-1,2 1/sec gemessen. Er betrug 13,3±1,0 cm HaO/l/sec, bzw. 14,44±1,0 cm H2O/l/sec. Der Widerstand der Endotrachealtuben und Verbindungsstucke entsprach 7-8 cm H2O/1/sec. Die inspiratorische Atem-arbeit variierte zwischen 0,55 und 1,31 kpm/min bei einer geschatzen Relation von 4:1 zwischen elastischer und Widerstandsarbeit. Die verwendeten Ventilationsvolumina fuhrten zu arteriellen Kohlensaurespannungswerten nahe um 40 mm Hg, womit der Wert einer Kalkulation der Ventilationsvolumina aus einem Spezialnomogramm bewiesen erscheint. Die alveolo-arteriellen Sauerstoffdruckunterschiede blieben in Normalbereichen (804±14 mm Hg, Bereich 28-143 mm Hg). Wahrend der Periode der kontrollierten Beatmung kam es zu keinem Absinken des arteriellen Sauerstoffdrucks und forcierte Aufblahung fuhrte zu keiner Verbesserung des Sauerstoffdruckwertes. Wir glauben, dass das besondere Stromungs-Druckmuster des Engstrom-Respirators-beschleunigender Gasstrom mit veranderlichem endinspiratorischen Druckplateau-jeder Tendenz zum Alveolarkollaps und moglicher Abnahme der Compliance entgegenwirkt. Diese Annahme wird understutzt durch experimentelle Untersuchungen, bei denen die Differenz zwischen der Verteilung insufflierter Volumina und Veranderungen der Compliance fur konstante und beschleunigende Gasstromungen analysiert wurden. Das variable endinspiratorische Druckplateau des Engstrom-Respirators vermittelt Zug fur Zug «Mini-seufzer», sodass keine Notwendigkeit besteht, diesen Apparat mit einem Spezialzusatz fur tiefe Seufzer auszustatten, wie dies kurzlich vorgeschlagen worden war. Unsere Befunde scheinen eine Erklarung dafur zu geben, warum andere Autoren, im Gegensatz zu uns, eine Abnahme der Compliance wahrend der kontrollierten Beatmung gefunden haben. Es war dies wahrscheinlich durch die Anwendung konstanter Gasstromungen und das Fehlen eines endinspiratorischen Plateaus, welche einen ungunstigen Effekt auf die Atemmechanik haben.

THE response of cerebral circulation to changes in arterial carbon dioxide tension (Paco 2 ) is well known and has been confirmed in numerous experiments and clinical observations. Nonetheless, the mechanism of the action of this gas is not completely understood although certain theories are presently generally accepted. The dilation of the cerebral vessels following an increase of Paco 2 is thought to be a result of the direct action of the gas on the smooth muscle in the cerebral arterial wall. 1-3 The observation of Cow in 1911 4 that isolated strips of carotid artery immersed in Ringer's solution dilate when CO 2 is dissolved in the medium is the principal justification for this theory. The possibility of a neural regulatory mechanism for the cerebral circulation has been widely assumed to be negligible or nonexistent because of failure of autonomic denervation or stimulation to affect cerebral blood flow (CBF)

Seventy episodes of status asthmaticus in 46 patients were treated in an acute respiratory care unit. These episodes were divided into three groups on the basis of admission arterial carbon dioxide tension (Paco 2 ) and response to treatment. In 28 episodes Paco 2 was less than 40 mm Hg. In 20 episodes Paco 2 was greater than 40 mm Hg. Both groups did not require intubation and were treated conservatively with intermittent positive pressure breathing, humidified oxygen, chest physiotherapy, and drugs. There were no deaths in these groups. Twenty-two episodes in which Paco 2 was greater than 40 mm Hg required treatment with intubation, drugs, and controlled mechanical ventilation. Two patients in this group died. The mortality is comparable to other large series treated in a similar fashion.