Arterial Carbon Dioxide Levels Research Articles

Down to the Wire? Ventilation during Intubated Stretcher Helicopter Winching

The stretcher winching of intubated patients into a helicopter is an uncommon procedure. Positive pressure ventilation is required, which can be performed either manually with a self-inflating bag or automatically using a mechanical ventilator. The optimal method of ventilation has not been studied. Automatic ventilation has theoretical advantages in maintaining better oxygenation and stable arterial carbon dioxide levels, with less risk of airway disconnection. There is also likely to be better performance and situational awareness of the stretcher attendant during the winch, contributing to crew and patient safety. However, the ability to diagnose and manage airway disconnections and ventilator failure is of concern. To compare automatic vs manual ventilation during intubated stretcher helicopter winching. There were 2 phases to the trial. An initial static winch with a hoisting simulator was performed with 10 stretcher attendants, followed by a live helicopter winch at 30 feet into a Bell 412 with 5 attendants. Each attendant performed 2 separate winches with an intubated mannequin. During one winch the mannequin was ventilated with manual (bag) ventilation; an automatic ventilator was used for the other. Airway pressures were measured. The results showed no failure of automatic ventilation. Automatic ventilation was superior to manual ventilation. Automatic ventilation allowed for better situational awareness and perceived performance in winching maneuvers. There was one airway disconnection during a manual ventilation winch into the aircraft. Automatic ventilation is superior in providing stable, reliable, uninterrupted ventilation during simulated helicopter winching. The risk of ventilator failure and disconnection is low. Medical retrieval organizations should develop standard operating procedures, equipment, and training to facilitate automatic ventilation during helicopter winching.

Noninvasive positive pressure ventilation for acute respiratory failure following upper abdominal surgery.

Each year, more than four million abdominal surgeries are performed in the US and over 250,000 in England. Acute respiratory failure, a common complication that can affect 30% to 50% of people after upper abdominal surgery, can lead to significant morbidity and mortality. Noninvasive ventilation has been associated with lower rates of tracheal intubation in adults with acute respiratory failure, thus reducing the incidence of complications and mortality. This review compared the effectiveness and safety of noninvasive positive pressure ventilation (NPPV) versus standard oxygen therapy in the treatment of acute respiratory failure after upper abdominal surgery. To assess the effectiveness and safety of noninvasive positive pressure ventilation (NPPV), that is, continuous positive airway pressure (CPAP) or bilevel NPPV, in reducing mortality and the rate of tracheal intubation in adults with acute respiratory failure after upper abdominal surgery, compared to standard therapy (oxygen therapy), and to assess changes in arterial blood gas levels, hospital and intensive care unit (ICU) length of stay, gastric insufflation, and anastomotic leakage. The date of the last search was 12 May 2015. We searched the following databases: the Cochrane Handbook for Systematic Reviews of Interventions (CENTRAL) (2015, Issue 5), MEDLINE (Ovid SP, 1966 to May 2015), EMBASE (Ovid SP, 1974 to May 2015); the physiotherapy evidence database (PEDro) (1999 to May 2015); the Cumulative Index to Nursing and Allied Health Literature (CINAHL, EBSCOhost, 1982 to May 2015), and LILACS (BIREME, 1986 to May 2015). We reviewed reference lists of included studies and contacted experts. We also searched grey literature sources. We checked databases of ongoing trials such as www.controlled-trials.com/ and www.trialscentral.org/. We did not apply language restrictions. We selected randomized or quasi-randomized controlled trials involving adults with acute respiratory failure after upper abdominal surgery who were treated with CPAP or bilevel NPPV with, or without, drug therapy as standard medical care, compared to adults treated with oxygen therapy with, or without, standard medical care. Two authors independently selected and abstracted data from eligible studies using a standardized form. We evaluated study quality by assessing allocation concealment; random sequence generation; incomplete outcome data; blinding of participants, personnel, and outcome assessors; selective reporting; and adherence to the intention-to-treat (ITT) principle. We included two trials involving 269 participants. The participants were mostly men (67%); the mean age was 65 years. The trials were conducted in China and Italy (one was a multicentre trial). Both trials included adults with acute respiratory failure after upper abdominal surgery. We judged both trials at high risk of bias. Compared to oxygen therapy, CPAP or bilevel NPPV may reduce the rate of tracheal intubation (risk ratio (RR) 0.25; 95% confidence interval (CI) 0.08 to 0.83; low quality evidence) with a number needed to treat for an additional beneficial outcome of 11. There was very low quality evidence that the intervention may also reduce ICU length of stay (mean difference (MD) -1.84 days; 95% CI -3.53 to -0.15). We found no differences for mortality (low quality evidence) and hospital length of stay. There was insufficient evidence to be certain that CPAP or NPPV had an effect on anastomotic leakage, pneumonia-related complications, and sepsis or infections. Findings from one trial of 60 participants suggested that bilevel NPPV, compared to oxygen therapy, may improve blood gas levels and blood pH one hour after the intervention (partial pressure of arterial oxygen (PaO2): MD 22.5 mm Hg; 95% CI 17.19 to 27.81; pH: MD 0.06; 95% CI 0.01 to 0.11; partial pressure of arterial carbon dioxide (PCO2) levels (MD -9.8 mm Hg; 95% CI -14.07 to -5.53). The trials included in this systematic review did not present data on the following outcomes that we intended to assess: gastric insufflation, fistulae, pneumothorax, bleeding, skin breakdown, eye irritation, sinus congestion, oronasal drying, and patient-ventilator asynchrony. The findings of this review indicate that CPAP or bilevel NPPV is an effective and safe intervention for the treatment of adults with acute respiratory failure after upper abdominal surgery. However, based on the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology, the quality of the evidence was low or very low. More good quality studies are needed to confirm these findings.

Management of pediatric traumatic brain injury.

Pediatric severe traumatic brain injury continues to be a major cause of disability and death. Rapid initial airway and hemodynamic stabilization is critical, followed by the need for immediate recognition of intracranial pathology that requires neurosurgical intervention. Intracranial hypertension and cerebral hypoperfusion have been recognized as major insults after trauma and management should be directed at preventing both. Sedation with opioids, moderate hyperventilation to arterial carbon dioxide level of 35-40mmHg, hyperosmolar therapy with 3% saline or mannitol, normothermia, and cerebrospinal fluid drainage continue to be the cornerstones of initial management of intracranial hypertension (intracranial pressure >20mmHg). Refractory intracranial hypertension is treated with high-dose barbiturate therapy to achieve medical burst suppression on electroencephalography and decompressive craniectomy. In addition, those children require antiepileptic medications for seizure prophylaxis, adequate nutritional management, and early physical therapy and rehabilitation referrals. Most of the evidence for care of children with brain injury comes from center-specific practice and experience rather than objective data. This lack of evidence provides the ground for ongoing research; nevertheless, outcomes after traumatic brain injury continue to show improvement.

Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats

Context: Air pollution exposure affects autonomic function, heart rate, blood pressure and left ventricular function. While the mechanism for these effects is uncertain, several studies have reported that air pollution exposure modifies activity of the carotid body, the major organ that senses changes in arterial oxygen and carbon dioxide levels, and elicits downstream changes in autonomic control and cardiac function.Objective: We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke and diesel exhaust, would activate the carotid body chemoreceptor response and lead to secondary cardiovascular responses in rats.Materials and methods: Spontaneously hypertensive (SH) rats were exposed once for 3 h to 3 ppm acrolein gas or filtered air in whole body plethysmograph chambers. To determine if the carotid body mediated acrolein-induced cardiovascular responses, rats were pretreated with an inhibitor of cystathionine γ-lyase (CSE), an enzyme essential for carotid body signal transduction.Results: Acrolein exposure induced several cardiovascular effects. Systolic, diastolic and mean arterial blood pressure increased during exposure, while cardiac contractility decreased 1 day after exposure. The cardiovascular effects were associated with decreases in pO2, breathing frequency and expiratory time, and increases in sympathetic tone during exposure followed by parasympathetic dominance after exposure. The CSE inhibitor prevented the cardiovascular effects of acrolein exposure.Discussion and conclusion: Pretreatment with the CSE inhibitor prevented the cardiovascular effects of acrolein, suggesting that the cardiovascular responses with acrolein may be mediated by carotid body-triggered changes in autonomic tone. (This abstract does not reflect EPA policy.)

Assessment of dynamic cerebral autoregulation and cerebral carbon dioxide reactivity during normothermic cardiopulmonary bypass.

Despite increased risk of neurological complications after cardiac surgery, monitoring of cerebral hemodynamics during cardiopulmonary bypass (CPB) is still not a common practice. Therefore, a technique to evaluate dynamic cerebral autoregulation and cerebral carbon dioxide reactivity (CO2R) during normothermic nonpulsatile CPB is presented. The technique uses continuous recording of invasive arterial blood pressure, middle cerebral artery blood flow velocity, absolute cerebral tissue oxygenation, in-line arterial carbon dioxide levels, and pump flow measurement in 37 adult male patients undergoing elective CPB. Cerebral autoregulation is estimated by transfer function analysis and the autoregulation index, based on the response to blood pressure variation induced by cyclic 6/min changes of indexed pump flow from 2.0 to 2.4 up to 2.8 L/min/m(2). CO2R was calculated from recordings of both cerebral blood flow velocity and cerebral tissue oxygenation. Cerebral autoregulation and CO2R were estimated at hypocapnia, normocapnia, and hypercapnia. CO2R was preserved during CPB, but significantly lower for hypocapnia compared with hypercapnia (p < 0.01). Conversely, cerebral autoregulation parameters such as gain, phase, and autoregulation index were significantly higher (p < 0.01) during hypocapnia compared with both normocapnia and hypercapnia. Assessing cerebral autoregulation and CO2R during CPB, by cyclic alteration of pump flow, showed an impaired cerebral autoregulation during hypercapnia.

Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways.

Emergency and difficult tracheal intubations are hazardous undertakings where successive laryngoscopy–hypoxaemia–re-oxygenation cycles can escalate to airway loss and the ‘can't intubate, can't ventilate’ scenario. Between 2013 and 2014, we extended the apnoea times of 25 patients with difficult airways who were undergoing general anaesthesia for hypopharyngeal or laryngotracheal surgery. This was achieved through continuous delivery of transnasal high-flow humidified oxygen, initially to provide pre-oxygenation, and continuing as post-oxygenation during intravenous induction of anaesthesia and neuromuscular blockade until a definitive airway was secured. Apnoea time commenced at administration of neuromuscular blockade and ended with commencement of jet ventilation, positive-pressure ventilation or recommencement of spontaneous ventilation. During this time, upper airway patency was maintained with jaw-thrust. Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) was used in 15 males and 10 females. Mean (SD [range]) age at treatment was 49 (15 [25–81]) years. The median (IQR [range]) Mallampati grade was 3 (2–3 [2–4]) and direct laryngoscopy grade was 3 (3–3 [2–4]). There were 12 obese patients and nine patients were stridulous. The median (IQR [range]) apnoea time was 14 (9–19 [5–65]) min. No patient experienced arterial desaturation < 90%. Mean (SD [range]) post-apnoea end-tidal (and in four patients, arterial) carbon dioxide level was 7.8 (2.4 [4.9–15.3]) kPa. The rate of increase in end-tidal carbon dioxide was 0.15 kPa.min−1. We conclude that THRIVE combines the benefits of ‘classical’ apnoeic oxygenation with continuous positive airway pressure and gaseous exchange through flow-dependent deadspace flushing. It has the potential to transform the practice of anaesthesia by changing the nature of securing a definitive airway in emergency and difficult intubations from a pressured stop–start process to a smooth and unhurried undertaking.

Obesity hypoventilation syndrome in Japan and independent determinants of arterial carbon dioxide levels.

Obesity hypoventilation syndrome (OHS) prevalence was previously estimated at 9% in patients with obstructive sleep apnoea (OSA) in Japan. However, the definition of OSA in that study was based on an apnoea-hypopnoea index (AHI) of ≥ 20/h rather than ≥ 5/h. Therefore, the prevalence of OHS in OSA was not measured in the same way as for Western countries. Our study objectives were to investigate the characteristics of Japanese patients with OHS. Nine hundred eighty-one consecutive patients investigated for suspected OSA were enrolled. At least 90% of them were from urban areas, including 162 with obese OSA (body mass index (BMI) ≥ 30 kg/m(2) and AHI ≥ 5/h). The prevalence of OHS (BMI 36.7 ± 4.9 kg/m(2) ) in OSA and that in obese OSA were 2.3% and 12.3%, respectively. Multiple regression analysis revealed that independent of age and BMI, arterial oxygen pressure (contribution rate (R(2) ) = 7.7%), 4% oxygen desaturation index (R(2) = 8.9%), carbon monoxide diffusing capacity/alveolar volume (R(2) = 8.3%), haemoglobin concentration (R(2) = 4.9%) and waist circumference (R(2) = 4.9%) were independently associated with arterial carbon dioxide pressure. After 12.3 ± 4.6 months of CPAP treatment, more than 60% of OHS patients no longer had hypercapnia. The prevalence of OHS in OSA in Japan was 2.3%. The mean BMI of patients with OHS in Japan was lower than that in Western countries (36.7 kg/m(2) vs 44.0 kg/m(2) ).

Continuing Professional Development: Capnography

Overview This Continuing Professional Development (CPD) Module will discuss the principles of partial pressures of gas, how the partial pressure of expired carbon dioxide is measured and review examples of the waveforms produced by ventilated patients. Learning Outcomes After completing this module you will be able to: • Define capnography and demonstrate an understanding of how it is recorded. • Discuss the merits and limitations of the three main ways of presenting capnography. • List the indications for capnography. • Describe the four phases of a normal capnograph waveform. • Develop an awareness of capnograph waveform deviations and misinterpretations. • Have an appreciation of how capnography relates to arterial carbon dioxide levels and the normal values.

Correlation of end tidal and arterial carbon dioxide levels in critically ill neonates and children.

Sir, We read with great interest the study titled “Correlation of end tidal and arterial carbon dioxide levels in critically ill neonates and children” by Mehta et al.[1] We wish to highlight certain important issues. It is not clear how the sample size was calculated for this study to reach to a fruitful conclusion as this was probably not a pilot study. We believe that without a priori calculation of sample size, it would be really impossible to draw conclusions. We observed a major discrepancy regarding the number of patients being enrolled and excluded from the study as evident from the flow chart in Figure 1 of the article published. In the neonatal arm, authors have excluded 21 patients, whereas the sum of excluded patients is 24. From the data provided by you, the number of patients would be 63 instead of 66, which would change the statistics as reported. Similarly, in the infant and children arm, of 10 pairs that were excluded, the cause of exclusion of two pairs is missing. In the neonatal arm, there were eight newborns (12%) suffering from congenital heart disease with left to right shunt. A large surgical shunt size is related to stiffer lungs and a large heart is associated with a higher respiratory resistance. During mechanical ventilation of patients, the end-tidal CO2 may be an unreliable substitute for arterial CO2. Studies have found a relationship between a decreased pulmonary to systemic shunt ratio and an increased arterial to end-tidal CO2 difference. This may indicate that a reason for the unreliability of end-tidal CO2 is an impaired gas exchange partially due to pulmonary hypoperfusion.[2] In the neonatal group, 68% of newborns were on vasoactive therapy. It is well established that the vasopressors actually decrease the pulmonary blood flow (PBF), which would have an adverse effect on the PaCO2 and PEtCO2 relationship. Also, it would have been more appropriate if the authors could have shown the dosage of vasopressors in the presence of shock/chronic heart failure in the severe acute respiratory distress syndrome group as it would have a significant bearing on the PBF and thereby on the ventilation. In newborns, mainstream sampling of the exhaled gas to monitor the EtCO2 was used, which has a dead space of around 6 mL. It is noteworthy that the mean weight of the neonate arm is 2.1 kg only as mentioned. In all the patients, we presume that a low tidal volume approach would have been applied as the ventilation strategy. Thus, the dead space would account for almost 40–50% of the exhaled air being analyzed by a mainstream sampler. We feel that low flow side-stream sampling would have been a more appropriate sampling tool in the neonate arm of this study as the significant dead space would be a confounding factor with regard to the result of the study.[2,3,4,5,6,7] Almost all the limitations highlighted are independent variables known to disrupt the positive correlation between PaCO2 and EtCO2. Hence, in our opinion, it would not be rational to conclude strongly that increased severity of lung disease as defined by P/F ratio < 200 negatively affects EtCO2 values in all age groups.

Correlation of end tidal and arterial carbon dioxide levels in critically Ill neonates and children.

Aim of the Study:End tidal carbon dioxide (EtCO2) monitoring is considered to reflect real-time estimation of partial pressure of carbon dioxide in arterial blood (PaCO2) noninvasively. However, knowledge about its relationship with PaCO2 in critically ill pediatric and neonatal patients is limited. The primary objective was to evaluate predictive capability of end tidal carbon dioxide monitoring and secondary objective was to determine the influence of severity of lung disease on EtCO2 and PaCO2 relationship.Materials and Methods:This was a prospective, nonrandomized, consecutive enrollment study carried out in neonatal and pediatric intensive care units of a tertiary care children hospital. It was conducted in 66 neonates and 35 children receiving mechanical ventilation. Severity of lung disease was estimated by ventilation index and PaO2/FiO2 (P/F) ratio. Simultaneous recording of EtCO2 and PaCO2 levels was done and data were analyzed for correlation and agreement.Results:In neonates, 150 EtCO2 and PaCO2 pairs were recorded. The mean weight ± SD of patients was 2.1 ± 0.63 kg. PaCO2 had a positive correlation with EtCO2 (r = 0.836, 95% CI = 0.78-0.88). P/F ratio <200 adversely affected relationship. In infants and children, 96 pairs were recorded. Mean age ± SD of patients was 4.20 ± 4.92 years and mean weight ± SD was 13.1 ± 9.49 kg. PaCO2 had an excellent correlation with EtCO2 (r = 0.914, 95% CI = 0.87 and 0.94). P/F ratio <200 adversely affected relationship.Conclusion:EtCO2 monitoring displayed a good validity to predict PaCO2. Correlation was affected by low P/F ratio (<200); hence, it is recommended that blood gases be measured in these patients until such time that a good relation can be established between end tidal and arterial CO2 values.

Correlation of end-tidal and arterial carbon-dioxide levels in critically Ill neonates and children.

Aim of the Study: End tidal carbon dioxide (EtCO 2 ) monitoring is considered to reflect real-time estimation of partial pressure of carbon dioxide in arterial blood (PaCO 2 ) noninvasively. However, knowledge about its relationship with PaCO 2 in critically ill pediatric and neonatal patients is limited. The primary objective was to evaluate predictive capability of end tidal carbon dioxide monitoring and secondary objective was to determine the influence of severity of lung disease on EtCO 2 and PaCO 2 relationship. Materials and Methods: This was a prospective, nonrandomized, consecutive enrollment study carried out in neonatal and pediatric intensive care units of a tertiary care children hospital. It was conducted in 66 neonates and 35 children receiving mechanical ventilation. Severity of lung disease was estimated by ventilation index and PaO 2 /FiO 2 (P/F) ratio. Simultaneous recording of EtCO 2 and PaCO 2 levels was done and data were analyzed for correlation and agreement. Results: In neonates , 150 EtCO 2 and PaCO 2 pairs were recorded. The mean weight ± SD of patients was 2.1 ± 0.63 kg. PaCO 2 had a positive correlation with EtCO 2 ( r = 0.836, 95% CI = 0.78-0.88). P/F ratio 2 had an excellent correlation with EtCO 2 ( r = 0.914, 95% CI = 0.87 and 0.94). P/F ratio Conclusion: EtCO 2 monitoring displayed a good validity to predict PaCO 2 . Correlation was affected by low P/F ratio ( 2 values.

Volume targeted ventilation and arterial carbon dioxide in extremely preterm infants

The aim of our study was to quantify arterial carbon dioxide levels (PaCO2) achieved by ventilating extremely preterm neonates in volume guarantee mode targeting tidal volumes of approximately 4 ml/kg. We performed a prospective trial on preterm infants with gestational age ≤28 weeks, birth-weight ≤1000 grams, postnatal age <48 hours and are supported by mechanical ventilation. All infants were ventilated using volume guarantee plus synchronized intermittent positive pressure ventilation (SIPPV + VG mode). Primary outcome was the average first PaCO2 in neonates and number of these infants with unacceptable first PaCO2. Pre-specified secondary outcomes were the average PaCO2 in infants ventilated during the first 48 hrs of ventilation and number of blood gases with an unacceptable PaCO2 in the first 48 hours. Sixty two infants were enrolled and 218 blood gases recorded up to 48 hours of age. The mean PaCO2 on the first arterial blood gas for infants ventilated in VG mode from admission to the nursery was 39.5 ± 6.3. The mean PaCO2 in the first 48 hours was 39.37 ± 6.99 mmHg. In our study, 91% of all PaCO2 values in the first 48 hours were between 35 and 60 mmHg. PaCO2 levels were in the acceptable range in 93% of infants at the time of first ABG measurement and in 91% of blood gases during the first 48 hours of ventilation. Newborn infants ventilated with volume guarantee ventilation targeting approximately 4 ml/kg of tidal volume, have acceptable PaCO2 levels at the first blood gas measurement and during the first 48 hours of ventilation.

Abstract 197: Initial Base Deficit and Arterial Carbon Dioxide Level Associated with Survival in Postarrest Patients

Introduction: Serial arterial blood gases (ABG) are typically monitored in post-arrest patients treated with therapeutic hypothermia (TH). The relationship between arterial carbon dioxide (PaCO 2 ) levels, degree of base deficit (BD), neurologic outcome, and survival is unclear. Hypothesis: Lower PaCO 2 , as a surrogate for hyperventilation, and larger BD, correlating with ongoing acidosis, may be associated with decreased survival and worse neurologic outcomes in post-arrest TH patients. Methods: We conducted a retrospective chart review of post-arrest patients treated with TH from the PATH database representing 11 institutions. Demographic variables were analyzed using chi-square tests. Unadjusted logistic regression analyses were performed to assess the relationship between hypocapnea (PaCO 2 &lt; 30 mmHg), normocapnea (PaCO 2 30-45 mmHg), hypercapnea (PaCO 2 &gt; 45 mmHg), mean BD, with respect to mortality or neurologic outcome at 1 st post-arrest ABG and at 6 hrs, 12 hrs, and 24 hrs post-arrest. Results: A total of 179 patients were enrolled. Patients were 59.6 ± 16.4 years, 54% male, and VF/VT was present in 31% of patients. Sixty-six (37%) survived to discharge, of which 76% (50/66) had a good neurologic outcome (CPC 1 or 2). Survivors had a lower mean initial PCO 2 value than non-survivors (49.0 vs. 57.5 mmHg; p=0.03); survival was significantly higher in patients who had normocapnea (51%) on their initial ABG when compared to those who were hypocapneic (25%) or hypercapneic (28%) (p=0.007), however, there was no significant difference in survival at the other time points. When adjusting for gender and initial rhythm, hypocapnea and hypercapnea had lower odds for survival in comparison to normocapnea (OR 0.23, 95% CI 0.03-2.01, p=0.18 and OR 0.72, 95% CI 0.35-1.5, p=0.38). Survivors had less severe BD than non-survivors at initial ABG (-8.0 vs. -11.3; p=0.005) and at all subsequent time points. There was no difference between PCO 2 or BD values between patients with good vs. bad neurologic outcomes. Conclusions: Patients who were normocapneic on initial ABG had improved survival. Survivors had lower initial PaCO 2 levels and less severe BD than non-survivors. There was no difference in PaCO 2 or BD values in patients with good vs. poor neurologic outcomes.

Using transcutaneous carbon dioxide monitor (TOSCA 500) to detect respiratory failure in patients with amyotrophic lateral sclerosis: A validation study

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition, respiratory failure being the commonest cause of death. Quality of life and survival can be improved by supporting respiratory function with non-invasive ventilation. Transcutaneous carbon dioxide monitoring is a non-invasive method of measuring arterial carbon dioxide levels enabling simple and efficient screening for respiratory failure. The aim of this study was to validate the accuracy of carbon dioxide level recorded transcutaneously with a TOSCA 500 monitor. It is a prospective, observational study of 40 consecutive patients with ALS, recruited from a specialist ALS clinic. The partial pressure of carbon dioxide (PCO(2)) in each patient was determined by both transcutaneous monitoring and by an arterialized ear lobe capillary blood sample. The carbon dioxide (CO(2)) levels obtained with these two methods were compared by Bland-Altman analysis. The results showed that the mean difference between arterialized and transcutaneous readings was - 0.083 kPa (SD 0.318). The Bland-Altman limits of agreement ranged from 0.553 to - 0.719 kPa. The difference was < 0.5 kPa in 90% of the recordings. Four of the 40 measurements had a difference of > 0.5 kPa, with a maximum recorded difference of 0.95 kPa. In conclusion, non-invasive carbon dioxide monitoring using a TOSCA monitor is a useful clinical tool in neurology practice. Users should be aware of the possibility of occasional inaccurate readings. A clinically unexpected or incompatible reading should be verified with a blood gas analysis, especially when a decision to provide ventilatory support is required.

Anesthesia Patient Safety Foundation Consensus Conference Report

Anesthesia Patient Safety Foundation Consensus Conference Report

POSITIVE END EXPIRATORY PRESSURE (PEEP);

Introduction: Thoracic surgeries and aesthesia for lung resection has presented anaesthesiologists with certain uniquephysiological problems. These include placing (lateral decubitus position) in order to obtain optimal access for most operations on lungs, pleura,esophagus, and great vessels, opening the chest wall (open pneumothorax) and one lung ventilation anaesthesia. One lung ventilationanaesthesia and lateral decubitus position produces decrease in functional residual capacity and an obligatory right to left shunt that rangesfrom 15% to 40% leading to increase in ventilation perfusion (V/Q) mismatch thus causing hypoxia and or hypoxemia. An optimal level ofpositive end expiratory pressure of 5cmH O when added to dependent lung is known to improve arterial oxygenation and improve ventilator 2efficiency. Objectives: To compare different values of positive end expiratory pressure (PEEP) during one lung ventilation, for its effects onblood arterial oxygenation and carbon dioxide levels. Study Design: Randomized controlled trial (RCT). Setting: Conducted in surgical Unit-IIIand Department of anaesthesia and Intensive Care, Combined Military Hospital, Rawalpindi. Duration of study with dates: Ten months from25-12-2008 to 01-10-2009, Additional quantum of Data was collected from 01-01-2011 to 25-01-2011. Subjects and methods: The patientswere divided into two equal groups of 100 patients each, by random allocation of patients to either in-group A (subjected to zero PEEP) or group-B (subjected to PEEP 5cm of water). Results: At induction and start of two lung ventilation 14 (14.0%) of the patients from group-A and 16(16.0%) from group-B had normal PaCO . At initiation of one lung ventilation 25 (25.0%) of the patients from group-A and 80 (80.0%) from group- 2B had normal PaO . At initiation of one lung ventilation 26 (26.0%) of the patients from group-A and 80 (80.0%) from group-B had normal PaCO 2 2with p &lt;0.001. At end of procedure one lung ventilation 30 (30.0%) of the patients from group-A and 90 (90.0%) from group-B had normal PaO . 2At end of procedure one lung ventilation 32 (32.0%) of the patients from group-A and 91 (91.0%) from group-B had normal PaCO . 2Conclusions: The execution of one-lung ventilation still constitutes a challenge in clinical and surgical practice.

Le pneumothorax tuberculeux (PT) : à propos de 29 cas

Background: Hypercapnic coma is a rare differential diagnosis in the unconscious patient. One underlying mechanism may be hypoventilation due to spontaneous pneumothorax. Although hypercapnia is not a typical finding in spontaneous pneumothorax in patients with otherwise healthy lungs, under certain circumstances, hypercapnia may readily develop. Objectives: We report a rare case of profound hypercapnic coma due to spontaneous pneumothorax after contralateral pneumonectomy. In addition, we review other causes of hypercapnic coma and its outcome and discuss the relationship between arterial carbon dioxide partial pressure and level of consciousness. Case Report: An 85-year-old man without evidence of trauma or intoxication presented unconscious to our Emergency Department. The physical examination and X-ray study revealed a left-sided spontaneous pneumothorax. A right-sided pneumonectomy 25 years earlier had promoted the development of profound hypercapnic coma. After insertion of a thoracic drain, the coma rapidly resolved without any neurological deficit. Conclusions: Although severe hypercapnia is usually due to decompensation of chronic lung disease, pneumothorax potentially may cause hypercapnic coma. Review of the literature suggests that there is no close correlation between arterial pCO2 (partial pressure of CO2) levels and the degree of impairment of consciousness; however, levels exceeding 80 mm Hg are likely associated with significantly impaired consciousness. Hypercapnic coma usually resolves without neurological deficit as arterial pCO2 tensions decline.

Opioids, Ventilation and Acute Pain Management

Despite the increasing use of a variety of different analgesic strategies, opioids continue as the mainstay for management of moderate to severe acute pain. However concerns remain about their potential adverse effects on ventilation. The most commonly used term, respiratory depression, only describes part of that risk. Opioid-induced ventilatory impairment (OIVI) is a more complete term encompassing opioid-induced central respiratory depression (decreased respiratory drive), decreased level of consciousness (sedation) and upper airway obstruction, all of which, alone or in combination, may result in decreased alveolar ventilation and increased arterial carbon dioxide levels. Concerns about OIVI are warranted, as deaths related to opioid administration in the acute pain setting continue to be reported. Risks are often said to be higher in patients with obstructive sleep apnoea. However, the tendency to use the term 'obstructive sleep apnoea' to encompass the much broader spectrum of sleep- and obesity-related hypoventilation syndromes and the related misuse of terminology in papers relating to obstructive sleep apnoea and sleep-disordered breathing remain significant problems in discussions of opioid-related effects. Opioids given for management of acute pain must be titrated to effect for each patient. However strategies aiming for better pain scores alone, without highlighting the need for appropriate monitoring of OIVI, can and will lead to an increase in adverse events. Therefore, all patients must be monitored appropriately for OIVI (at the very least using sedation scores as a '6th vital sign') so that it can be detected at an early stage and appropriate interventions triggered.

Can mainstream end-tidal carbon dioxide measurement accurately predict the arterial carbon dioxide level of patients with acute dyspnea in ED

ObjectiveThis study was designed to determine whether the mainstream end-tidal carbon dioxide (ETCO2) measurement can accurately predict the partial arterial carbon dioxide (Paco2) level of patients presented to emergency department (ED) with acute dyspnea. MethodsThis prospective, observational study was conducted at a university hospital ED, which serves more than 110 000 patients annually. Nonintubated adult patients presented with acute dyspnea who required arterial blood gas analysis were recruited in the study for a 6-month period between January and July 2010. Patients were asked to breathe through an airway adapter attached to the mainstream capnometer. Arterial blood gas samples were obtained simultaneously. ResultsWe included 162 patients during the study period. The mean ETCO2 level was 39.47 ± 10.84 mm Hg (minimum, 19 mm Hg; maximum, 82 mm Hg), and mean Paco2 level was 38.95 ± 12.27 mm Hg (minimum, 16 mm Hg; maximum, 94 mm Hg). There was a positive, strong, statistically significant correlation between ETCO2 and Paco2 (r = 0.911, P < .001). The Bland-Altman plot shows the mean bias ± SD between ETCO2 and Paco2 as 0.5 ± 5 mm Hg (95% confidence interval, −1.3165-0.2680) and the limits of agreement as −10.5 and +9.5 mm Hg. Eighty percent (n = 129) of the ETCO2 measurements were between the range of ±5 mm Hg. ConclusionMainstream ETCO2 measurement accurately predicts the arterial Paco2 of patients presented to ED with acute dyspnea. Further studies comparing mainstream and sidestream methods in these patients are required.

Noninvasive Capnometry for End-tidal Carbon Dioxide Monitoring via Nasal Cannula in Nonintubated Neonates

Arterial blood gas analysis is the gold standard for assessing the adequacy of ventilation. However, arterial blood sampling may be associated with serious complications in neonates. The aim of the study was to utilize the side-stream capnometry measurement of end-tidal carbon dioxide (PetCO₂) via nasal cannula circuits and to verify the reliability of PetCO₂ in reflecting the arterial blood carbon dioxide(PaCO₂) level in nonintubated neonates. A retrospective medical record review analysis was performed in nonintubated neonates admitted to the neonatal ward in a medical center. Simultaneous arterial PaCO₂ and PetCO₂ levels were evaluated. PaCO₂ and PetCO₂ levels were compared by paired t test and were correlated using Pearson's correlation. The PetCO₂ bias was defined as the difference between PaCO₂ and PetCO₂, and was assessed by Bland-Altman plot analysis. A total of 34 neonates were recruited, and data of 54 pairs of PaCO₂ and PetCO₂ levels were available for comparison. The average (mean ± SD) gestational age was 32.5 ± 4.2 weeks, and the average birth weight was 1881 ± 1077 g. There was a good correlation between PetCO₂ and PaCO₂ levels among all paired samples (r = 0.809, p < 0.001). When the data were divided into those with respiratory disease (n = 34) and those without (n = 20), significant correlation between PetCO₂ and PaCO₂ levels were both noted in the former group (r = 0.823, p < 0.001) and the latter group (r = 0.770, p < 0.001). The overall average mean value of PetCO₂ was lower than that of PaCO₂ (39.4 ± 8.8 mmHg vs. 41.3 ± 9.2 mmHg, p = 0.014). The difference between PetCO₂ and PaCO₂ levels was significant only among those with respiratory disease (38.8 ± 9.8 mmHg vs. 41.2 ± 10.3 mmHg, p = 0.027), but not among those without (40.5 ± 7.0 mmHg vs. 41.6 ± 7.2 mmHg, p = 0.289). End-tidal CO₂ measurement by side-stream capnometry through nasal cannula could provide an accurate and noninvasive estimate of PaCO₂ levels in nonintubated neonates.