Search

Background In this prospective observational study, we evaluated the effects of fluid bolus (FB) on venous-to-arterial carbon dioxide tension (PvaCO2) in 42 adult critically ill patients with pre-infusion PvaCO2 > 6 mmHg. Results FB caused a decrease in PvaCO2, from 8.7 [7.6−10.9] mmHg to 6.9 [5.8−8.6] mmHg (p < 0.01). PvaCO2 decreased independently of pre-infusion cardiac index and PvaCO2 changes during FB were not correlated with changes in central venous oxygen saturation (ScvO2) whatever pre-infusion CI. Pre-infusion levels of PvaCO2 were inversely correlated with decreases in PvaCO2 during FB and a pre-infusion PvaCO2 value < 7.7 mmHg could exclude a decrease in PvaCO2 during FB (AUC: 0.79, 95%CI 0.64–0.93; Sensitivity, 91%; Specificity, 55%; p < 0.01). Conclusions Fluid bolus decreased abnormal PvaCO2 levels independently of pre-infusion CI. Low baseline PvaCO2 values suggest that a positive response to FB is unlikely., SCOPUS: ar.j, info:eu-repo/semantics/published

So far, only a few studies have examined and confirmed the correlation between end-expiratory carbon dioxide partial pressure (PETCO2) and arterial carbon dioxide tension (PaCO2) during invasive mechanical ventilation in critically ill patients. This study aimed to observe the correlation between PaCO2 and PETCO2 in patients on invasive mechanical ventilation. This was a cross-sectional study of adult patients on invasive mechanical ventilation enrolled between June 2018 and March 2019. Patients requiring invasive mechanical ventilation underwent one of the following mechanical ventilation modes: assisted/controlled ventilation, synchronized intermittent mandatory ventilation, and spontaneous breathing. Subsequently, the difference and correlation between PETCO2 and PaCO2 were analyzed. A total of 184 patients with 298 pairs of PETCO2-PaCO2 data were included in the analysis. Without distinguishing the ventilator mode, there was significant positive correlation between PETCO2 and PaCO2. In different ventilator modes, the correlation coefficient was 0.81 for synchronized intermittent mandatory ventilation, 0.47 for assisted/controlled ventilation, and 0.55 for spontaneous breathing, respectively. In patients with chronic obstructive pulmonary disease (r = 0.80), multiple trauma (r = 0.64), severe pneumonia (r = 0.60), gastrointestinal surgery (r = 0.57), and cerebrovascular diseases (r = 0.53), PETCO2 and PaCO2 were positively correlated. For oxygenation index

Study objectives To determine the relationships between partial pressure of arterial carbon dioxide (PaCO 2 ), prescribed minute ventilation (MV), and neurologic outcome in patients resuscitated from cardiac arrest. Methods This was a retrospective cohort study utilizing a multicenter database of adult patients with return of spontaneous circulation (ROSC) after cardiac arrest. The primary outcome was neurologic status at hospital discharge, defined by Cerebral Performance Category (CPC) score: CPC 1–2 was favorable, CPC 3–5 was poor. We compared rates of initial normocarbia (PaCO 2 31–49mmHg) and mean sequential PaCO 2 measurements obtained over the first 24h. We also assessed the influence of MV on the PaCO 2 at initial, 6, 12, 18, and 24h after cardiac arrest using univariate linear regression. Results One hundred and fourteen patients from 3 institutions met inclusion criteria. Overall, 46/114 (40.4%, 95% CI: 31.4–49.4%) patients survived to hospital discharge, and 33/114 (28.9%, 20.6–37.2%) had CPC 1–2 at the time of discharge. A total of 38.9% (95% CI: 29.9–47.9%) of patients had initial normocarbia; 43.2% (28.6–57.8%) of these patients were discharged with CPC 1–2, compared with 20.3% (10.8–29.8%) of dyscarbic patients. By 6h, neurologic outcomes were not significantly associated with PaCO 2 . Prescribed MV was not associated with PaCO 2 at any time point with the exception of a weak correlation at hour 18. Conclusion Initial normocarbia was associated with favorable neurological outcome in patients resuscitated from cardiac arrest. This relationship was not seen at subsequent time points. There was no significant association between prescribed MV and PaCO 2 or neurologic outcome.

Introduction Arterial carbon dioxide tension (PaCO 2 ) abnormalities are common after cardiac arrest (CA). Maintaining a normal PaCO 2 makes physiological sense and is recommended as a therapeutic target after CA, but few studies have examined the association between PaCO 2 and patient outcomes. This systematic review and meta-analysis aimed to assess the effect of a low or high PaCO 2 on patient outcomes after CA. Methods We searched MEDLINE, EMBASE, CINAHL and Cochrane CENTRAL, for studies that evaluated the association between PaCO 2 and outcomes after CA. The primary outcome was hospital survival. Secondary outcomes included neurological status at the end of each study's follow up period, hospital discharge destination and 30-day survival. Meta-analysis was conducted if statistical heterogeneity was low. Results The systematic review included nine studies; eight provided sufficient quantitative data for meta-analysis. Using PaCO 2 cut-points of 45mmHg to define hypo- and hypercarbia, normocarbia was associated with increased hospital survival (odds ratio [OR] 1.30, 95% confidence interval [CI] 1.23, 1.38). Normocarbia was also associated with a good neurological outcome (cerebral performance category score 1 or 2) compared to hypercarbia (OR 1.69, 95% CI 1.13, 2.51) when the analysis also included an additional study with a slightly different definition for normocarbia (PaCO 2 30–50mmHg). Conclusions From the limited data it appears PaCO 2 has an important U-shape association with survival and outcomes after CA, consistent with international resuscitation guidelines' recommendation that normocarbia be targeted during post-resuscitation care.

Hypocarbia during the first 12 h of life is associated with mortality and disability in neonatal hypoxic ischemic encephalopathy (HIE). Notable variation in arterial carbon dioxide tension (PaCO2) during the first 4 d of life is related to severe intraventricular hemorrhages in preterm infants. We examined the association between PaCO2 during 72 h of whole-body therapeutic hypothermia for neonatal HIE and 2-year neurodevelopmental outcomes.A retrospective review of 23 term neonates treated with whole-body hypothermia documented clinical, demographic and arterial blood gas data. Comparisons were made across good and severe neurodevelopmental outcome groups at 2 years of age.Severe neurodevelopmental outcomes were documented in 8 of 23 toddlers. There were no significant differences between outcome groups with regard to the number of patients with hypocarbic means or measurements. There were also no significant differences with mean PaCO2, PaO2, pH, time-weighted cumulative hypocarbia, and PaCO2 range. The severe neurodevelopmental outcomes group had a significantly higher mean PaCO2 standard deviation (p = 0.04; 95% CI, -5.46 to -0.39).Severe neurodevelopmental outcomes were significantly associated with high PaCO2 variability over 72 h in whole-body-cooled HIE neonates. Mitigating these fluctuations may be a potential management strategy.

Aim The harmful effect of hypocapnia on the neonatal brain emphasizes the importance of monitoring arterial carbon dioxide tension (PaCO2). Transcutaneous monitoring of carbon dioxide (tcPCO2) reduces the need for arterial blood sampling. Drawbacks are high electrode temperature causing risks of skin burning. The aim was to determine the accuracy and precision of tcPCO2 at reduced electrode temperature. Methods Forty newborns (GA 24.9-41.7) were included. Two tc-monitors were applied (TCM4, Radiometer, Copenhagen). Arterial blood gas sampling and monitoring of tcPCO2-level at different electrode temperatures was done simultaneously (39°C, 40°C, 41 °C, 42°C, 44°C). Difference of PaCO2-tcPCO2 was expressed as a percentage of the mean. Results Mean PaCO2 was 5.8kPa [3,2; 7.9]. Bias (PaCO2 -tcPCO2) increased from 5% at 44°C to 17% at 39°C, but did not differ significantly between 41°C and 40°C. The precision of the tcPCO2 at each temperature ranged from +7-10%. After correction for the temperature-dependent over-reading, we found increasing PaCO2 — tcPCO2 difference with increasing PaCO2, approx. 2% pr. kPa increase of CO2. Only mild transient erythema was observed. Conclusion A lower electrode temperature in tcPCO2-monitoring increases systematic overreading of the tc-electrode. However, in very preterm babies, monitoring at 40°C or 41°C is possible provided a bias correction of 12-15% is applied.

Objectives: To assess the appropriateness of arterial carbon dioxide tension control in a group of 92 patients with traumatic brain injury who, despite receiving advanced prehospital care, showed no improved outcome in comparison with a group homogeneous but for a lower level of prehospital care. Methods: A retrospective registration of the early in-hospital arterial carbon dioxide tension of the patients intubated and ventilated on scene. Patients were excluded if the arterial carbon dioxide tension did not reflect prehospital ventilation or its alteration might have been intentional or unavoidable. Results: Arterial carbon dioxide tension was normal (35-45 mmHg) in only six of the 16 suitable cases (37.5%), was elevated (>45 mmHg) in three cases (18.75%), low (25-35 mmHg) in five cases (31.25%), and extremely low (

Supplemental Digital Content is available in the text, The objective of this study was to examine the repeatability of blood gas (BG) parameters and their derived variables such as the central venous-to-arterial carbon dioxide tension difference (▵Pco2) and the ratio of ▵Pco2 over the central arteriovenous oxygen content difference (▵Pco2/C(a-cv)O2) and to determine the smallest detectable changes in individual patients. A total of 192 patients with arterial and central venous catheters were included prospectively. Two subsequent arterial and central venous blood samples were collected immediately one after the other and analyzed using the same point-of-care BG analyzer. The samples were analyzed for arterial and venous BG parameters, ▵Pco2, and ▵Pco2/C(a-cv)O2 ratio. Repeatability was expressed as the smallest detectable difference (SDD) and the least significant change (LSC). A change in value of these parameters exceeding the SDD or the LSC should be regarded as real. The SDDs for arterial carbon dioxide tension, arterial oxygen saturation, central venous oxygen saturation (ScvO2), and ▵Pco2 were small: ±2.06 mm Hg, ±1.23%, 2.92%, and ±1.98 mm Hg, respectively, whereas the SDDs for arterial oxygen tension (Pao2) and ▵Pco2/C(a-cv)O2 were high: ±9.09 mm Hg and ±0.57 mm Hg/mL, respectively. The LSCs (%) for these variables were 5.06, 1.27, 4.44, 32.4, 9.51, and 38.5, respectively. The repeatability of all these variables was good except for Pao2 and ▵Pco2/C(a-cv)O2 ratio for which we observed an important inherent variability. Expressed as SDD, a ScvO2 change value of at least ±3% should be considered as true. The clinician must be aware that an apparent change in these variables in an individual patient might represent only an inherent variation.

We compared the accuracy and reliability of a validated, physiological simulator and six intensive care specialists in predicting changes in arterial oxygen tension (PaO(2)), arterial carbon dioxide tension (PaCO(2)) and pH following adjustment of mechanical ventilation. Twenty-five data sets were collected before and after routine alterations in ventilator settings. Fractional inspired oxygen was adjusted in all patients and minute volume was adjusted in 13 patients. The simulator was more accurate and consistent than all the physicians in predicting the magnitude of PaO(2) and pH change. The simulator had a larger bias in estimating the magnitude of change of PaCO(2) than four of the physicians, but was more consistent than all but one of the physicians. The simulator may prove to be a useful tool in the management of mechanical ventilation. Incorporation into mechanical ventilators in a passive predictive role or an active 'closed-loop' ventilation management system are potential roles for physiological simulation.

The effect of modified ultrafiltration (MUF) after cardiopulmonary bypass for paediatric cardiac surgery was evaluated in 138 children with moderate to severe congenital heart disease. The median age was 0.4 years (0 days to 6.5 years), and the weight 5.3 kg (2.2-20 kg). The operation was discontinued in six cases, three because of technical problems and three because of unstable circulation. One-hundred-and-thirty-four patients were ultrafiltrated for a median of 12 min (2-27 min) with an ultrafiltrate of median 44 ml/kg (6-118 ml/kg). Haematocrit was significantly increased from 28% (20-39%) to 36% (26-51%) and systolic arterial pressure from 56 mmHg (30-85 mmHg) to 74.0 mmHg (32-118 mmHg). Furthermore arterial oxygenation was significantly increased from 30.8 kPa (4.8-70.4 kPa) to 34.1 kPa (4.9-80.6 kPa), and arterial carbon dioxide tension from 4.8 kPa (3.1-7.3 kPa) to 5.1 kPa (3.1-7.6 kPa). Heart rate was significantly reduced from 145 beats/min (92-201 beats/min) to 136 beats/min (88-200 beats/min). There were no significant differences in central venous pressure, left atrial pressure and base excess before and after MUF. MUF increases systolic blood pressure, haematocrit, arterial oxygen and carbon dioxide tension coming off bypass in paediatric cardiac surgery and reduces heart rate and postoperative fluid overload.

To investigate changes of cerebral arteriovenous oxygen content difference (AVDO2) induced by surgical incision and to determine carbon dioxide (CO2) reactivity of the cerebral circulation during sevoflurane and isoflurane anaesthesia. Twenty-one ASA 1–2 patients undergoing elective surgery for supratentorial tumours were randomly allocated to receive either 1.3 MAC sevoflurane/N2O anaesthesia (n =10) or equi-MAC isoflurane/N2O anaesthesia (n = 11). Before and after incision, haemodynamic measurements and AVDO2 determinations were performed. After opening the dura, AVDO2 was determined before and after the respiration rate was increased by 50%. Incision produced an increase in mean arterial pressure from 69 ±11 to 97 ±22 mmHg (mean ±SD) (P < 0.0005) and from 71 ±6 to 89 ±12 mmHg (P < 0.0001) in the sevoflurane and isoflurane groups, respectively, whereas the heart rate increased from 60 ±9 to 72 ±8 bpm (P < 0.001) and from 65 ±6 to 70 ±7 bpm (P < 0.001), respectively. Arterial carbon dioxide tension (PaCO2) was increased from 33.6 ±2.3 to 34.6 ±1.8 mmHg (P < 0.05) with incision in the sevoflurane group. The AVDO2 was decreased from 6.5 ±1.6 to 5.3 ±1.6 vol% (P < 0.0005) in the sevoflurane group and from 6.7 ±1.1 to 6.0 ±1.1 vol% (P < 0.01) in the isoflurane group. The % change of AVDO2 was larger in the sevoflurane group than in the isoflurane group (−18.3 ±8.4% vs −9.1 ±9.0%; P < 0.05) but no difference remained after the postincisional AVDO2 value of the sevoflurane group was corrected for pre-incisional PaCO2. Carbon dioxide reactivity, calculated as the percent change in AVDO2 per mmHg change in PaCO2, was 6.1 ±3.0% mmHg−1 in the sevoflurane group and 5.9 ±2.4% · mmHg−1 in the isoflurane group (P = NS). Sevoflurane and isoflurane are associated with similar impairment of cerebral flow-metabolism coupling at incision, while CO2 reactivity is maintained during both anaesthetics. Etudier les changements de la difference arterioveineuse du contenu en oxygene cerebral (AVDO2) produits par l’incision et determiner la reactivite au gaz carbonique (CO2) de la circulation cerebrale sous anesthesie au sevoflurane et a l’isoflurane. Vingt et un patients ASA 1 et 2 subissant une chirurgie non urgente pour tumeur supratentorielle ont ete aleatoirement assignes a recevoir soit une anesthesie au sevoflurane/N2O 1,3 MAC (n = 10) soit une anesthesie a l’isoflurane/N2O equi-MAC (n = 11). Avant et apres l’incision, les mesures hemodynamiques ont ete effectuees et AVDO2 determinee. Apres l’ouverture de la dure-mere, AVDO2 a ete calculee avant et apres une augmentation de la frequence respiratoire de 50%. L’incision a provoque une augmentation de la pression arterielle moyenne respective de 69 ±11 a 97 ±22 mmHg (moyenne ±ET) (P < 0,0005) et 71 ±6 a 89 ±12 (P < 0,0001) dans les groupes sevoflurane et isoflurane; la frequence cardiaque augmentait respectivement de 60 ±9 a 72 ±8 bpm (P < 0,001) et de 65 ±6 a 70 ±7 bpm (P < 0,001). Dans le groupe sevoflurane, la PaCO2 augmentait de 33,6 ±2,3 a 34,6 ±1,8 (P < 0,05) avec l’incision. Dans le groupe sevoflurane, AVDO2 diminuait de 6,5 ±1,6 a 5,3 ±1,6 vol% (P < 0,0005) et dans le groupe isoflurane, de 6,7 ±1,1 a 6,0 ±1,1 vol% (P < 0,01). Le pourcentage de changement de AVDO2 etait plus important dans le groupe sevoflurane que dans le groupe isoflurane (−18,3 ±8,4% vs −9,1 ±9,0%; P < 0,05); cette difference est disparue une fois la valeur post-incision du groupe sevoflurane corrigee pour la valeur de PaCO2 pre-incision. La reactivite du gaz carbonique, calculee en pourcentage de changement en AVDO2 par mmHg de changement de PaCO2 etait 6,1 ±3,0% · mmHg−1 dans le groupe sevoflurane et 5,9 ±2,4% · mmHg−1 dans le groupe isoflurane (P = NS). Le sevoflurane et l’isoflurane sont associes a une perturbation identique du couplage debit-metabolisme a l’incision, alors que la reactivite au CO2 est maintenue avec les deux anesthesiques.

Jugular bulb oximetry provides the first bedside available information on cerebral oxygen utilization. An extensive analysis was made of all initial jugular bulb oximetry data obtained in 150 patients within the first 12 h after severe traumatic brain' injury. These data revealed initial abnormal jugular bulb saturation values in 57 patients (= 38% of study population), with a predominance of jugular bulb desaturation (observed in 45 patients). This confirms earlier reports that revealed a high incidence of disturbed and inadequate cerebral perfusion in the first hours after brain injury. Jugular bulb desaturation was especially related to systemic causes (such as a lowered cerebral perfusion pressure observed in 29 patients, and a lowered arterial carbon dioxide tension in 24 patients). These findings could have important implications for the emergency management of severely head-injured patients, as outcome might possibly be improved by better attention to all systemic factors that might reduce cerebral perfusion in the early hours after traumatic insult.

There is much controversy about the optimal bloodgas management of hypothermic patients, whether the hypothermia is caused by accidents or induced before operations. The surgeons and anestesiologists have acquired more clinical experience the last years when operating patients in hypothermia. The comparative physiology has given increased information about the blood gas strategy of heterothermic endotherms and poikilothermic ectotherms during lowering of their core temperature. There are two types of strategies which have been used in clinical medicine the last years in the blood gas management of patients in hypothermia: pH-stat method and alpha-stat method. In the pH-stat method, the arterial carbon dioxide tension (pCO2(a)) is maintained at 5.3 kPa (40 mmHg) and the pH is maintained at 7.40 when measured at the actual temperature. It is then necessary to add CO2 to the inspired gas. In the alpha-method, the arterial carbon dioxide tension and the pH are maintained at 5.3 kPa and 7.40 when measured at +37 degrees C. When a patient is cooled down, the pH-value will increase and the pCO2-value and the pO2-value will decrease with lowering of the temperature if measured at the patients temperature. Both the pH-stat and alpha-stat strategies have theoretical disadvantages. For the optimal myocardial function the alpha-stat method is the method of choice. The pH-stat method may result in loss of autoregulation in the brain (coupling of the cerebral blood flow with the metabolic rate in the brain). By increasing the cerebral blood flow beyond the metabolic requirements, the pH-stat method may lead to cerebral microembolisation and intracranial hypertension. In Norway the alpha-stat strategy is the preferred method.

The difference between mixed venous blood carbon dioxide tension (PvCO(2)) and arterial carbon dioxide tension (PaCO(2)), called ∆PCO(2) has been proposed to better characterize the hemodynamic status. It depends on the global carbon dioxide (CO(2)) production, on cardiac output and on the complex relation between CO(2) tension and CO(2) content. The aim of this review is to detail the physiological background allowing adequate interpretation of ∆PCO(2) at the bedside. Clinical and experimental data support the use of ∆PCO(2) as a valuable help in the decision-making process in patients with hemodynamic instability. The difference between central venous CO(2) tension and arterial CO(2) tension, which is easy to obtain can substitute for ∆PCO(2) to assess the adequacy of cardiac output. Differences between local tissue CO(2) tension and arterial CO(2) tension can also be obtained and provide data on the adequacy of local blood flow to the local metabolic conditions.

Study A lipid emulsion containing 10 percent medium-chain triglycerides (MCT) and 10 percent long-chain triglycerides (LCT) was infused at a rate of 1 ml/kg/h (3.3 mg/kg/min) for 2 h, in 12 patients (2 males, 10 females; mean age, 54 ± 3 (SEM) years; range, 34 to 67 years) 24 h after open-heart surgery (mitral valve replacement). Methods Hemodynamic factors (pulmonary and radial artery indwelling catheters), oxygen and carbon dioxide partial pressures, oxygen saturation, oxygen delivery and consumption, and intrapulmonary shunt fraction were obtained before, during, and after lipid infusion (for 2 h), at 30-s intervals, along with some metabolic indexes (triglycerides, free fatty acids, glucose, insulin, lactate, acetoacetate). Results No statistically significant changes in heart rate, cardiac index, systemic and pulmonary pressures and resistances, central venous and pulmonary capillary pressures, or arterial oxygen partial pressure were observed during infusion. Arterial carbon dioxide partial pressure values were constantly reduced throughout and after the end of lipid infusion, as compared with baseline values, while oxygen consumption was increased significantly without any change in oxygen delivery. No adverse effects on intrapulmonary shunt fraction were observed. Statistically significant increases of triglycerides, free fatty acids, acetoacetate and insulin (peak values at end of the lipid infusion) were found in comparison with baseline values. Plasma glucose increased significantly during lipid infusion and remained higher than baseline values until the end of the study. Lactate levels were unchanged, except for a slight decrease at the end of the study, without any derangement of acid-base equilibrium. Neither arrhythmias nor adverse clinical reactions were observed as a consequence of lipid infusion. Conclusion Fat emulsions containing both MCT and LCT, when given at 3.3 mg/kg/min for 120 min following valvular heart surgery, do not exert negative cardiopulmonary effects, and could represent a source of rapidly metabolized substrates.

End-tidal carbon dioxide tension (PetCO2) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on PetCO2 being an accurate surrogate for arterial carbon dioxide tension (PaCO2), the latter being the physiologically relevant variable. This study tested the hypothesis that PetCO2 provides an accurate assessment of PaCO2 during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress ( N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in PetCO2 ( N = 7). PetCO2 and PaCO2 decreased during heat stress ( P < 0.001); however, there was no group difference between PaCO2 and PetCO2 ( P = 0.36) nor was there a significant interaction between thermal condition and measurement technique ( P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, PetCO2 and PaCO2 at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between PaCO2 and PetCO2 while normothermic ( P = 0.14) and following a 1.0 ± 0.2°C ( P = 0.21) and 1.4 ± 0.2°C ( P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of PetCO2 and PaCO2 were similar ( P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in PetCO2 (7.5 ± 2.8 mmHg) and PaCO2 (6.6 ± 3.4 mmHg) were similar ( P = 0.31). These data indicate that mean PetCO2 reflects mean PaCO2 during the evaluated conditions.

Objective: Cheyne Stokes respiration (CSR) is frequently seen in the patients with heart failure (HF) and it increases mortality. In the present study, we aimed to evaluate acute effects of adaptive servo ventilation (ASV) on CSR and neurohormones in the patients with HF. Methods: Nineteen males and 1 female patients with HF in the functional capacity of NYHA II-III were included into the study prospectively. One night polysomnography (PSG) was performed to all patients. In addition to medical treatment, 10 patients having CSR were applied ASV in another night together with PSG.. Arterial blood gases, plasma epinephrine and norepinephrine, serum N-terminal -pro-B type brain natriuretic peptide (NT-pro-BNP) were studied in the first night and after ASV treatment. A Wilcoxon test was used for comparison of parameters before and after treatment; and Mann-Whitney-U test was used for comparison of parameters between the patients with CSR and without CSR. Results: Mean age of 10 patients with CSR was 62.2±11.1 years. Their etiologies were ischemic in 9 patients and idiopathic dilated cardiomyopathy in 1 patient. While there were no significant differences in the levels of PaCO2, HCO3, PH, before and after treatment; PaO2 (75.3 mmHg) and SatO2 (94.7%) significantly increased after the therapy (84.7 mmHg, 96.5% and p=0.007 and p=0.008 respectively). While NT-proBNP (3029.6±1450.5 pg/ml), norepinephrine (625.4±304.7 pg/ml) and epinephrine (65.4±24.1 pg/ml) were higher than normal before ASV treatment, all of them showed significant reductions after treatment (1694.0±925.9 pg/mvl, 333.9±165.4 pg/ml and 45.0±20.5 pg/ml; p=0.005, p=0.005 and p=0.02, respectively). Conclusions: One night ASV treatment improves CSR, partial pressure of oxygen in arterial blood, and oxygen saturation and provides significant reductions in plasma catecholamines and NT-proBNP levels in the patients with HF and CSR. Prospective studies are needed to evaluate long-term effects of ASV treatment on morbidity and mortality in the patients with HF. © Copyright 2009 by AVES Yayincilik Ltd.

To the Editors: Obesity hypoventilation syndrome (OHS) is commonly defined as a combination of obesity (body mass index (BMI) >30 kg·m−2), waking arterial hypercapnia (arterial carbon dioxide tension ( P a,CO2) >6.0 kPa (45 mmHg)) and sleep-disordered breathing. Essential to the diagnosis is exclusion of other causes of alveolar hypoventilation 1. The lack of a standardised definition of OHS in general, and of OHS–obstructive sleep apnoea relationships in particular, leads to confusion. One of the main aspects that has not been clarified is the assessment of OHS severity. This appears to be directly related to the degree of hypercapnia, the degree of hypoxaemia and the presence of complications 2, 3. Nevertheless, …

The aim of this study was to evaluate the influence on cerebral and cutaneous vascular regions of PaO2 reduction during acetate dialysis, by monitoring conjunctival oxygen tension (PcjO2) and Transcutaneous oxygen tension (PtcO2) during hemodialysis (HD) treatment. The study was performed on 23 patients with end-stage renal disease in chronic HD. All patients underwent dialytic treatment with cuprophan membranes and acetate containing dialysate. PcjO2 and PtcO2 were recorded and Pao2 and arterial carbon dioxide tension (PaCO2) were also measured. Results of the study show that hypoxemia during acetate dialysis with cuprophan membranes is not accompanied by changes of PcjO2 and therefore by changes in cerebral oxygenation. Moreover, PtcO2 remains constant during dialysis treatment. Furthermore, maintenance of normal oxygen tension at the conjunctival level is not obtained at the expense of the peripheral region of the skin.

BACKGROUND: The Laryngeal Tube (LT), (VBM Medizintechnik, Sulz, Germany) is a relatively new supraglottic device for controlling the airway. Arterial carbon dioxide tension (PaCO(2)) can be estimated by monitoring the end-tidal tension of carbon dioxide (PETCO(2)). The relationship between PETCO(2) and PaCO(2) during controlled ventilation via the LT has not been reported. METHODS: During general anesthesia, 45 patients were mechanically ventilated using an LT. PETCO(2) and PaCO(2) were measured once PETCO(2) had reached a steady state. The LT was then removed and the trachea intubated using an endotracheal tube (ETT), and the identical ventilatory variables were resumed. Following stabilization, PETCO(2) was again determined and PaCO(2) estimated. RESULTS: The mean PETCO(2) and PaCO(2) values were 4.43 +/- 0.26 kPa and 4.67 +/- 0.32 kPa, respectively, during LT ventilation, and 4.36 +/- 0.23 kPa and 4.61 +/- 0.26 kPa, respectively, during ETT ventilation. Analysis of differences between the PETCO(2) and PaCO(2) values using the Bland and Altman method revealed a bias +/- precision of 0.24 +/- 0.15 kPa for LT and 0.27 +/- 0.15 kPa for ETT. The root mean square error was 0.28 for the LT and 0.30 for the ETT. CONCLUSION: This study suggests that for healthy adult patients mechanically ventilated via the LT, the PETCO(2) value reflects the PaCO(2) value as closely as when patients are ETT ventilated, allowing capnometry to be used to evaluate the adequacy of ventilation.

In recent years, noncomprehensive "guidelines" were proposed for the management of severe acute brain injuries, focusing strictly on two approaches: 1) to maintain cerebral perfusion pressure anywhere above 70 mm Hg; and 2) to maintain arterial carbon dioxide tension levels above 30 torr. Strictly following these propositions, a recently reported prospective controlled study addressed mortality rates of no less than 75-76%, far worse than mortality rates reported before those "guidelines" were published. As a humanitarian alternative, the present comprehensive guidelines are aimed at addressing practical bedside strategies to manage no only intracranial pressure and cerebral perfusion pressure but also cerebral extraction of oxygen, based on solid previously reported papers which revealed the lowest mortality rates (below 15%) in the pertinent literature, in recent years. Em anos recentes, "diretrizes" não abrangentes foram propostas para o tratamento de traumatismos cerebrais agudos graves, enfocando estritamente em duas abordagens: 1) manter-se a pressão de perfusão cerebral em quaisquer níveis acima de 70 mm Hg; e 2) manter-se a pressão parcial de gás carbônico arterial acima de 30 torr. Seguindo estritamente tais proposições, artigo recentemente publicado envolvendo estudo prospectivo controlado revelou taxas de mortalidade de não menos que 75-76%, muitissímo piores do que taxas de mortalidade publicadas anteriormente a essas "diretrizes". Como uma alternativa humanitária, as diretrizes aqui propostas têm como meta explicar estrategias para que se tratem não apenas a pressão intracraniana e a pressão de perfusão cerebral, mas também a extração cerebral de oxigênio, baseando-se em trabalhos sólidos publicados anteriormente, os quais revelaram as menores taxas de mortalidade (inferiores a 15%) da literatura pertinente, em anos recentes.

We compared the effects of liquid and vaporized dry heparin on neonatal arterial blood gases. A total of 35 paired simultaneously drawn neonatal arterial blood samples were collected. In one of every paired sample, 0.05 cc of liquid heparin was used and in the other sample vaporized heparin syringes were used. Blood was drawn into every syringe to a total volume of 0.2 ml, pH, arterial oxygen tension (PaO2), and arterial carbon dioxide tension (PaCO2) of the paired samples were analyzed using the paired Student t method. There was no statistical difference in pH and PaO2 but the PaCO2 was statistically lower (p less than 0.0005) with liquid heparin. We conclude that the effects of heparin on neonatal arterial blood gases is dilutional in nature and that they are due to mixing heparin with its very low PaCO2 with the blood sample. If by mistake more heparin than necessary is used, the effects can be dramatic. We therefore suggest using syringes with vaporized heparin in obtaining neonatal arterial blood gases to obtain reliable and consistent results.

The jugular bulb oxygen saturation (SjO 2 ) and end-tidal carbon dioxide (ETCO 2 ) were monitored continuously during surgery in six cases of Moyamoya disease who had demonstrated multiple episodes of transient ischemic attacks (TIAs) and/or fluctuating neurological deficits preoperatively. The arterial carbon dioxide tension (PaCO 2 ) levels were also measured repeatedly at predetermined interval. In two cases (group H), the ETCO 2 was controlled at hypercapnic levels during surgery (45.5±1.5 mmHg) and the remaining four (group N) were operated on in a normocapnic state (39.0±2.0 mmHg). The group H patients demonstrated high levels of SjO 2 ranging from 72 to 85%, indicative of excessive hyperemia. One of the group H patients demonstrated mild and transient motor weakness postoperatively. The group N patients demonstrated normal levels of SjO 2 ranging from 66 to 78%. All the patients in both groups demonstrated fluctuations in SjO 2 levels in clear positive correlation with spontaneous changes in PaCO 2 levels. The present findings indicated that: (1) Global carbon dioxide reactivity of cerebral perfusion is well preserved in patients with Moyamoya disease; and (2) hypercapnia in these patients often causes excessive hyperemia. The occurrence of postoperative neurological deficits in association with such an excessive hyperemia suggests that hyperapnia during surgery is not always beneficial. Intraoperative monitoring of SjO 2 is useful for maintaining cerebral perfusion within the optimum range.

The most commonly used mode of noninvasive mechanical ventilation (NMV) is volume-controlled intermittent positive pressure ventilation (IPPV). Pressure support ventilation has recently become increasingly popular, but its merits have not been clearly defined. In an open, nonrandomized follow-up study, we evaluated two modes of NMV, volume-controlled (IPPV) and pressure-controlled ventilation (PCV) over 6 months in 30 consecutive patients (24 males and 6 females, aged 49 +/- 19 yrs) with chronic respiratory failure (CRF). The baseline assessments comprised both physiological and subjective data. In all cases, nasal IPPV was initially administered for 1 month, followed by a second month of nasal PCV. Thereafter, responders or nonresponders to PCV were defined according to the patients' subjective symptom score and/or the recurrence of hypercapnia. During the IPPV phase, in all but two patients the subjective and objective parameters improved significantly. During the following 1 month PCV phase, stabilization was maintained in 18 patients ("responders"), while 10 patients were defined as "nonresponders". In nonresponders, hypercapnia increased (arterial carbon dioxide tension (Pa,CO2): 5.7 +/- 0.4 to 6.6 +/- 0.5 kPa; p < 0.05) and symptom scores decreased. Compared with responders, nonresponders had a lower mean nocturnal arterial oxygen saturation (Sa,O2) (p < 0.05) and a higher daytime Pa,CO2 (p < 0.05) at baseline. We con clude that the majority of patients suffering from chronic respiratory failure who are initially satisfactorily ventilated with intermittent positive pressure ventilation may also be adequately maintained with pressure-controlled ventilation. However, there is a subgroup with more severe chronic respiratory failure at baseline, in whom pressure-controlled ventilation is inadequate. After 4 weeks of treatment with pressure-controlled ventilation, the subjective scores and the arterial carbon dioxide tension values reliably distinguished between long-term responders and nonresponders to pressure-controlled ventilation.

The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation.To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived.There was a fall in fractional dead space ventilation (0.43 to 0.28; P0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension.The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.

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

The response of cerebral blood volume (CBVR) to a small induced change in arterial carbon dioxide tension was studied by near-infrared spectroscopy in 17 newborn infants born from 26 wk of gestation to term. All 17 infants were undergoing mechanical ventilation but had apparently normal brains. The CBVR per kPa change in arterial carbon dioxide tension within the range 3.9 to 9.6 kPa was calculated from the change in total cerebral Hb concentration ([TCHb]) using the equation: delta CBV = delta [TCHb] x 0.89/[H] where [H] is the large vessel Hb concentration. A least-squares regression line with 95% confidence limits was derived for CBVR against gestational age. A highly significant linear increase in CBVR was found: mean CBVR from the regression increased from 0.07 mL.100 g-1.kPa-1 at 26 wk to 0.51 mL.100 g-1.kPa-1 at 40 wk.

We describe a patient with the hypokalemic type of familial periodic paralysis (FPP) who received atracurium for muscle relaxation as required for diagnostic laparoscopy. Electrocardiographic (EKG) T-wave changes suggestive o f hypokalemia were not supported by blood determinations. Arterial blood measurements of potassium (K + ), pH, and arterial carbon dioxide tension (PaCO 2 ) and the patient's esophageal temperature were maintained within normal limits. The degree of muscle relaxation was closely monitored by a peripheral nerve stimulator and train-of four (TOF) measurement of muscle twitch height. At the conclusion of the surgical procedure, no reversal to the muscle relaxant was needed or given. The patient regained preoperative muscle strength, and her postoperative course was uneventful.

End-tidal carbon dioxide (ETCO2) values obtained from awake nonintubated patients may prove to be useful in estimating a patient’s ventilatory status. This study examined the relationship between arterial carbon dioxide tension (PaCO2) and ETCO2 during the preoperative period in 20 premedicated patients undergoing various surgical procedures. ETCO2 was sampled from a 16-gauge intravenous catheter pierced through one of the two nasal oxygen prongs and measured at various oxygen flow rates (2, 4, and 6 L/min) by an on-line ETCO2 monitor with analog display. Both peak and time-averaged values for ETCO2 were recorded. The results showed that the peak ETCO2 values (mean = 38.8 mm Hg) correlated more closely with the PaCO2 values (mean = 38.8 mm Hg; correlation coefficient r = 0.76) than did the average ETCO2 values irrespective of the oxygen flow rates. The time-averaged PaCO2-ETCO2 difference was significantly greater than the PaCO2-peak ETCO2 difference (P < 0.001). Values for subgroups within the patient population were also analyzed, and it was shown that patients with minute respiratory rates greater than 20 but less than 30 and patients age 65 years or older did not differ from the overall studied patient population with regard to PaCO2-ETCO2 difference. A small subset of patients with respiratory rates of 30/ min or greater (n = 30) did show a significant increase in the PaCO2-ETCO2 difference (P < 0.001). It was concluded that under the conditions of this study, peak ETCO2 values did correlate with PaCO2 values and were not significantly affected by oxygen flow rate. However, obtaining peak ETCO2 values is clinically more difficult, especially when partial air-way obstruction is present.

This paper presents a method of controlling the arte- rial carbon dioxide tension of patients receiving mechanical venti- lation. Controlling of the CO tension is achieved by regulating the ventilator initiated breath frequency and also volume per breath.

The duration of action of atracurium was studied in two groups of patients. In group I (n = 15), patients' lungs were hyperventilated to a mean PaCO2 of 3.3 kPa and in group II (n = 15) lungs were ventilated to maintain a mean PaCO2 of 5.3 kPa. Anaesthesia was maintained using an infusion of propofol. The time taken to return to a T1 twitch height of 10% of control was measured following each incremental dose of atracurium 0.15 mg kg-1. It was found that the duration of action of atracurium was significantly (P less than 0.0005) shorter in the hypocapnic group.

A rapid, simple method for predicting the arterial oxygen tension (PaO 2 ) at any fractional concentration of inspired oxygen (FIo 2 ) is presented. The method is based on a nomogram interrelating PaO 2 , arterial carbon dioxide tension (PaCO 2 ) and FIo2, allowing rapid determination of the arterial to alveolar oxygen tension ratio a/A P02. The applicability of the nomogram and its reliability for predicting the PaO 2 at any FIo2 were studied prospectively in nine consecutive patients requiring mechanical ventilation (16 trials). On each occasion, a desired PaO 2 was chosen and from the nomogram an FIo 2 expected to yield this PaO 2 was administered. The PaO 2 was then measured. Actual PaO 2 differed from desired PaO 2 by a mean of 2.6 mm Hg (range 0 to 10 mm Hg, standard deviation (SD) 4.8). Retrospectively, we analyzed the nomogram's ability to predict the PaO 2 ± 9.6 mm Hg (2 SD) at varying FI0 2 . The overall sensitivity of this method was 85 percent (126 predictions out of 149 trials). We conclude that appropriate levels of supplemental oxygen can be rapidly and reliably chosen using the nomogram in selected patients.

The relationship between arterial carbon dioxide tension and end tidal carbon dioxide tension was studied in 19 patients during general anaesthesia for Caesarean section. Thirteen patients scheduled for elective abdominal hysterectomy formed a nonpregnant group. There was significant correlation between arterial and end tidal CO2 tensions in both groups. During Caesarean section, this difference was significantly less than in the nonpregnant group.

We have studied the serial changes in arterial blood gases in fourteen patients with acute severe asthma, all of whom received a standard therapeutic regime and had similar measurements made at identical time intervals under standard conditions. Hypoxaemia on admission was a constant finding, and the arterial oxygen tension often took a week or longer to return to a normal level. Treatment with 60% inspired oxygen provided a safe means of relieving hypoxaemia, provided that blood gases were measured before and during oxygen therapy. Most patients had a normal arterial carbon dioxide tension, which indicated the severity of their illness. Acid-base disturbances, when present, were mild and needed no specific treatment. Age, duration of the acute attack, and severity of airways obstruction were all unrelated to the changes in blood gas tension, and pulse rate was found to be a poor predictor of hypoxaemia in elderly asthmatics. Serial measurements of the arterial blood gases should be made in all patients with acute severe asthma.

The effect on the arterial carbon dioxide tension of assisting spontaneously breathing patients under halothane anaesthesia has been studied. A reduction in PaCO2 is usually seen, but it was reduced below 40 torr in only 30 per cent of cases, while a rise was recorded in 20 per cent.

✓ Ninety-three endarterectomies for carotid stenosis were monitored with cerebral blood flow (CBF) measurements, and 113 with both CBF measurements and a continuous electroencephalogram (EEG). Significant CBF increase occurred only when carotid endarterectomy was for a stenosis greater than 90%. A high correlation between CBF and EEG indicated when a shunt was required. To sustain a normal EEG, the CBF ascertained by the initial slope technique must be 18 ml/100 gm/min at an arterial carbon dioxide tension (PaCO2) of 40 torr. The degree of EEG change below this level during occlusion reflected the severity of reduced blood flow and was reversible with replacement of a shunt. The value and limitations of these monitoring techniques and a concept of ischemic tolerance and critical CBF are discussed.

To achieve normocarbia during conventional mechanical ventilation, ventilator settings are determined initially on the basis of body weight. The best ventilator settings for CO2 elimination during high-frequency jet ventilation (HFJV) have not been so clearly defined. A recent study has suggested that eucarbia will be obtained with HFJV when tidal volume (VT) per kg of body weight is kept within a narrow, well-defined range. In the same study, a "bench test" demonstrated that VT was directly proportional to the jet ventilator driving pressure (DP). The goal of our study was to confirm this recommended VT/kg to obtain eucarbia and to determine whether the relation observed between VT and DP in the laboratory was true clinically. We studied 14 patients admitted to the ICU for postoperative support. We determined a good correlation between DP and VT/kg (r = .811, p less than .001) for the group as a whole and a good inverse correlation between DP or VT/kg and PaCO2 for most individual patients; however, there was a poor inverse correlation between DP or VT/kg and PaCO2 for the group as a whole, due to wide patient-to-patient variation in the efficiency of jet ventilation. We conclude that there is no universal formula for setting jet ventilator DP or VT/kg to affect normocarbia in humans.

Based on measurements of arterial CO2 tension in 132 adult patients, a curve was constructed relating fresh gas inflow and arterial CO2 tension for a modified Mapleson D system. In patients on controlled ventilation using a ventilating volume greater than the predicted respiratory minute volume, it was found that the arterial Pco2 can be predicted from the fresh gas inflow with an accuracy sufficient to be clinically useful.

A method for obtaining carotid back pressures at the time of cerebral angiography is described. These preoperative measurements were compared to intraoperative measurements in 18 patients. Preoperative mean carotid back pressures (usually common carotid pressures) were obtained by occluding the artery with a double-lumen balloon catheter and recording the pressure distal to the balloon. Although the mean arterial blood pressure and the arterial carbon dioxide tension proved to be variables, the correlation of the pressures measured at angiography and at surgery was high (p less than 0.001).

When the syndrome consisting of sleep-induced apnea and hypersomnolence is due to upper airway obstruction, the hypersomnolence is believed to be the direct result of deprivation of sleep related to such obstructions. The purpose of this report is to describe a group of four asymptomatic subjects with upper airway obstruction during sleep. These subjects were matched with a group of patients with the syndrome of sleep-induced apnea and hypersomnolence. There were no significant differences between symptomatic and asymptomatic groups in terms of the absolute number of upper airway obstructions (252 vs 231), their mean duration (20.8 vs 25.9 seconds), the mean arterial carbon dioxide tension during sleep (39 vs 39 mm Hg), or the electroencephalographic patterns during sleep. The only variables that emerged as significantly different between the two groups were the weights (128 vs 90 kg; P less than 0.05), the low arterial oxygen pressure (PaO2) on waking (54 vs 80 mm Hg; P less than 0.002), and the lower PaO2 during sleep (47 vs 70 mm Hg; P less than 0.01) in the symptomatic patients. From these data, we conclude that the hypersomnolence in patients with sleep-induced apnea due to upper airway obstruction cannot be explained by deprivation of sleep, and other factors need to be carefully examined in future studies.

The precision of an interpretation of gas exchange records in progressive exercise is limited by the typical breath-to-breath variation in the data. Recently, two procedures have been proposed for minimizing the "noise" in the estimates of alveolar gas exchange time series data. One approach utilizes an estimate of pulmonary blood flow (Q) for smoothing purposes. The other approach utilizes an estimate of effective lung volume (V'L) for smoothing purposes. In this paper, we formulate the smoothing problem as a general linear model and demonstrate the concurrent estimates of both V'L and Q. Furthermore, we investigate the interaction between V'L and Q. Specifically, when a high value of lung volume is used (such as the subject's resting functional residual capacity) in the alveolar gas exchange algorithm, the estimate of Q is biased low and the result is a less effective smoothing of the data. In addition, we demonstrate how the Q estimate can be improved by utilizing more appropriate estimates of arterial carbon dioxide tension.

The effect of administration of terbutaline on the pulmonary and cardiovascular systems was studied in ten children with status asthmaticus. Terbutaline (0.01 to 0.04 mg/kg of body weight) was given subcutaneously in multiple doses. A significant decrease in respiratory rate and in arterial blood pressure, with no significant change in cardiac rate, was seen only after the first dose of terbutaline. There was a decrease in mean arterial carbon dioxide tension and an increase in mean arterial oxygen pressure. There was gross clinical improvement following administration of terbutaline in nine of the ten patients. One patient who failed to respond to administration of terbutaline also failed to respond to intravenously administered isoproterenol. We conclude that terbutaline is effective in the treatment of status asthmaticus, with only modest effects on the cardiovascular system.

The influence of some components of the tobacco smoke on the vestibulo-ocular reflex arc was studied. In accordance with a previous report it was shown that tobacco smoking provoked an obvious increase of the vestibular nystagmus frequency while the speed of the slow components remained unchanged. The injection of nicotine intravenously gave a similar change in the nystagmus pattern as was obtained after smoking. An increase in the carboxy-hemoglobin content by smoking a nicotine-free cigarette did not change the vestibular nystagmus pattern. An elevation of the arterial carbon dioxide tension affected the vestibular nystagmus only slightly, and in an opposite way compared to smoking. The results indicate that nicotine is the main component in the tobacco smoke responsible for the changes in the nystagmus pattern observed after smoking. There is evidence that the effects observed are due to changes in neuronal transmission of the vestibulo-ocular reflex arc.

SUMMARY General anaesthesia was given to 63 in-patients for electroconvulsive therapy. The relaxant-modified method, using thiopentone and suxamethonium, was used on 134 occasions. For 220 treatments methohexitone, without suxamethonium, was used a graded potential stimulus being applied instead of an instantaneous maximal electrical stimulus. Comparing the two methods it was found that there were significantly fewer increases in blood pressure and an absence of dental or oral trauma with the methohexitone technique. The results of arterial blood-gas analysis of 15 patients treated by this technique showed that there was neither a dangerous fall in arterial oxygen tension nor a marked rise in arterial carbon dioxide tension.

Blood gases, tidal volumes, and respiratory rates were measured preoperatively and during surgery with intermittent positive pressure breathing of 50 per cent oxygen. The ventilator was set to provide a tidal volume and rate closely approximating that in the awake state.

The Suwa nomogram was devised to predict the amount of mechanical dead space which must be added to a ventilated patient’s breathing circuit to achieve a normal arterial carbon dioxide tension of 40 mm Hg from a hypocapnoeiac level. The reliability of the mathematical analysis from which the nomogram was derived, together with the Suwa nomogram itself, were assessed in nine patients in respiratory failure. The results from 26 samples verified the mathematical analysis with a difference of ± 1 mm Hg from the predicted value of 40 mm Hg for arterial carbon dioxide tension when mechanical dead space was added. The mechanical dead space predicted by the Suwa nomogram to achieve an arterial carbon dioxide tension of 40 mm Hg was shown to have a potential error of ± 3.23 mm Hg. It was shown that the mathematical analysis warranted more use than the Suwa nomogram because of superior accuracy.