A prolonged postinspiratory pause enhances CO2 elimination by reducing airway dead space

Background: CO₂ elimination per breath (V_CO2,T) depends primarily on tidal volume (V_T). The time course of flow during inspiration influences distribution and diffusive mixing of V_T and is therefore a secondary factor determining gas exchange. To study the effect of a postinspiratory pause we defined ‘mean distribution time’ (MDT) as the mean time given to inspired gas for distribution and diffusive mixing within the lungs. The objective was to quantify changes in airway dead space (V_Daw), slope of the alveolar plateau (SLOPE) and V_CO2,T as a function of MDT in healthy pigs. Methods: Ten healthy pigs were mechanically ventilated. Airway pressure, flow and partial pressure of CO₂ were recorded during resetting of the postinspiratory pause from 10% (baseline) to, in random order, 0, 5, 20 and 30% of the respiratory cycle. The immediate changes in V_Daw, SLOPE, V_CO2,T, and MDT after resetting were analyzed. Results: V _Daw in percent of V_T decreased from 29 to 22%, SLOPE from 0·35 to 0·16 kPa per 100 ml as MDT increased from 0·51 to 1·39 s. Over the same MDT range, V_CO2,T increased by 10%. All these changes were statistically significant. Conclusion: MDT allows comparison of different patterns of inspiration on V_Daw and gas exchange. Estimation of the effects of an altered ventilator setting on exchange of CO₂ can be done only after about 30 minutes, while the transient changes in V_CO2,T may give immediate information. MDT affects gas exchange to an important extent. Further studies in human subjects in health and in disease are needed.     

Does End‐tidal Carbon Dioxide Monitoring Detect Respiratory Events Prior to Current Sedation Monitoring Practices?

Objectives: The value of ventilation monitoring with end‐tidal carbon dioxide (ETCO₂) to anticipate acute respiratory events during emergency department (ED) procedural sedation and analgesia (PSA) is unclear. The authors sought to determine if ETCO₂ monitoring would reveal findings indicating an acute respiratory event earlier than indicated by current monitoring practices. Methods: The study included a prospective convenience sample of ED patients undergoing PSA. Clinicians performed ED PSA procedures with generally accepted patient monitoring, including oxygen saturation (SpO₂), and clinical ventilation assessment. A study investigator recorded ETCO₂ levels and respiratory events during each PSA procedure, with clinical providers blinded to ETCO₂ levels. Acute respiratory events were defined as SpO₂≤92%, increases in the amount of supplemental oxygen provided, use of bag‐valve mask or oral/nasal airway for ventilatory assistance, repositioning or airway alignment maneuvers, and use of physical or verbal means to stimulate patients with depressed ventilation or apnea, and reversal agent administration. Results: Enrollment was stopped after independent review of 20 acute respiratory events in 60 patient sedation encounters (33%). Abnormal ETCO₂ findings were documented in 36 patients (60%). Seventeen patients (85%) with acute respiratory events demonstrated ETCO₂ findings indicative of hypoventilation or apnea during PSA. Abnormal ETCO₂ findings were documented before changes in SpO₂ or clinically observed hypoventilation in 14 patients (70%) with acute respiratory events. Conclusions: Abnormal ETCO₂ findings were observed with many acute respiratory events. A majority of patients with acute respiratory events had ETCO₂ abnormalities that occurred before oxygen desaturation or observed hypoventilation.     

Assessment and Monitoring of Pediatric Procedural Sedation

As emergency medicine physicians and other nonanesthesiologists continue to take more prominent roles in pediatric PSA, the significance of a standardized approach to insure patient safety becomes paramount. Appropriate preparation includes the recognition of sedation as a continuum and assembling equipment and trained staff accordingly. A detailed focused assessment of the child will help to identify those at risk for adverse events. This assessment will further help the practitioner decide which PSA medication regimen is most appropriate, as well as the most appropriate timing and setting for the procedure. Although no clear relationship exists between preprocedural fasting and increased adverse outcomes, appropriate assessment and risk-benefit analysis should be completed. Informed consent of parents and clarification of sedation expectations remain an important part of any preprocedural routine. Finally, newer modalities such as Etco₂ and BIS monitoring are quickly enhancing the safety of PSA when used as adjuncts to standard pulse oximetry and hemodynamic monitoring parameters.     

Increased Cerebral Blood Flow And Cardiac Output Following Cerebral Arterial Air Embolism In Sheep

1. The effects of cerebral arterial gas embolism on cerebral blood flow and systemic cardiovascular parameters were assessed in anaesthetized sheep. 2. Six sheep received a 2.5 mL injection of air simultaneously into each common carotid artery over 5 s. Mean arterial blood pressure, heart rate, end-tidal carbon dioxide and an ultrasonic Doppler index of cerebral blood flow were monitored continuously. Cardiac output was determined by periodic thermodilution. 3. Intracarotid injection of air produced an immediate drop in mean cerebral blood flow. This drop was transient and mean cerebral blood flow subsequently increased to 151% before declining slowly to baseline. Coincident with the increased cerebral blood flow was a sustained increase in mean cardiac output to 161% of baseline. Mean arterial blood pressure, heart rate and end-tidal carbon dioxide were not significantly altered by the intracarotid injection of air. 4. The increased cardiac output is a pathological response to impact of arterial air bubbles on the brain, possibly the brainstem. The increased cerebral blood flow is probably the result of the increased cardiac output and dilation of cerebral resistance vessels caused by the passage of air bubbles.     

Volumetric or time‐based capnography for excluding pulmonary embolism in outpatients?

Summary. Background: Volumetric capnography is technically more demanding but theoretically better than the time‐based alveolar deadspace fraction (P_aco ₂ – Etco ₂)/P_aco ₂ as a bedside diagnostic tool for excluding pulmonary embolism (PE) in outpatients. Objective: We compared both diagnostic accuracy in patients with a suspected PE and positive D‐dimer enzyme‐linked immunosorbent assay results. Patients and methods: In this clinical multicenter trial with prospective inclusion and 3‐month follow‐up, alveolar deadspace fraction was compared by receiver operating characteristic (ROC) analysis with other parameters derived from volumetric capnography. Results: Capnography was performed in 239 patients, and 205 tests (86%) were conclusive. The incidence of PE was 33%. The alveolar deadspace fraction accuracy expressed with ROC curve analysis was 0.73 ± 0.04. The diagnostic performances of parameters from volumetric capnography were not significantly better. Sixteen per cent [95% confidence interval (CI) 12–21%] of patients presented a (P_aco ₂ – Etco ₂)/P_aco ₂ ratio under the cut‐off value of 0.15, with a low clinical probability. This combination excluded PE, with a sensitivity of 96% (95% CI 89–99%) and a negative likelihood ratio of 0.17 (95% CI 0.09–0.33%). Conclusion: Volumetric capnography failed to show superiority to alveolar deadspace fraction measurements [(P_aco ₂ – Etco ₂)/P_aco ₂] for exclusion of PE in outpatients with positive D‐dimer test results. Future studies should clarify the safety of excluding PE in patients combining low clinical probability with positive D‐dimer results and (P_aco ₂ – Etco ₂)/P_aco ₂ ratios below the cut‐off value of 0.15.     

Alveolar Dead Space as a Predictor of Severity of Pulmonary Embolism

OBJECTIVE: To determine whether the alveolar dead space volume (V(D)alv), expressed as a percentage of the alveolar tidal volume (V(D)alv/V(T)alv), can predict the degree of vascular occlusion caused by pulmonary embolism (PE). METHODS: Fifty-three subjects with suspected PE were prospectively studied. Pulmonary embolism was diagnosed in 33 by high-probability ventilation/perfusion (V/Q) scan (n = 19) or by pulmonary arteriography (PAG, n = 14). Pulmonary embolism was excluded by PAG in 20 subjects. The V(D)alv/V(T)alv was determined from volumetric capnography and arterial blood gas analysis, which permits measurement of the physiologic dead space, V(D)phys (mL) = [(PaCO2 - PeCO2)/PaCO2]. tidal volume. Airway dead space (V(D)aw) was subtracted to yield the alveolar dead space [(V(D)phys - V(D)aw) = V(D)alv (mL)]; the percentage of alveolar volume occupied by alveolar dead space per breath = V(D)alv/V(T)alv x 100%. Percentage perfusion defect was determined from V/Q scans by a radiologist blinded to other data. Regression analysis was performed to show correlation between V(D)alv/V(T)alv and defect on V/Q scan or systolic pulmonary arterial pressure (SPAP). RESULTS: For subjects with PE, the mean perfusion defect on lung scan was 38 +/- 22%; the mean V(D)alv = 208 +/- 115 mL, V(T)alv = 452 +/- 251 mL, and V(D)alv/V(T)alv = 43 +/- 18%. Regression of V(D)alv/V(T)alv vs perfusion defect yielded r2 = 0.41. Regression of V(D)alv/V(T)alv vs pulmonary artery pressures yielded r2 = 0.59. For subjects without PE, V(D)alv/V(T)alv = 27 +/- 14% and V(D)alv = 89 +/- 66 mL. CONCLUSIONS: The V(D)alv/V(T)alv correlates with the lung perfusion defect and the pulmonary artery pressures in subjects with PE. These findings show the potential for V(D)alv/V(T)alv to quantify the embolic burden of PE.     

Detection of tracheal malpositioning of nasogastric tubes using endotracheal cuff pressure measurement

BACKGROUND: Insertion of a gastric tube (GT) in anaesthetized, paralyzed and intubated patients may be difficult. Tracheobronchial malposition of a GT may result in deleterious consequences. The purpose of this study was to determine the reliability of tracheal cuff pressure measurement to detect endobronchial malposition of GTs. We compared this new method with the measurement of exhaled CO(2) through the GT. METHODS: Thirty patients under general anesthesia and orotracheal intubation were analysed. First, the cuff pressure of the low-volume endotracheal tube (ET; ID 7.0-8.5 mm) was increased to 40 cmH(2)O. Then, in a randomized fashion, the GT (18 Charrière) was inserted consecutively into the trachea and oesophagus or vice versa. Cuff pressure was monitored continuously while advancing the GT. Furthermore, a capnograph was connected to the gastric tube and the aspirated PCO(2) was monitored. RESULTS: Advancement of the gastric tube into the oesophagus increased ET cuff pressure by 1 +/- 1 cmH(2)O, while endotracheal placement of the GT increased cuff pressure by 28 +/- 8 cmH(2)O (P < 0.001). Using an increase of >10 cmH(2)O in cuff pressure detected endotracheal malpositioning of the GT with 100% sensitivity and specificity. In 28 out of 30 cases, PCO(2) increased by more than 2.6 kPa. Thus, the PCO(2) approach failed to detect tracheal malpositioning in two cases resulting in a sensitivity of 93.3%. CONCLUSIONS: In intubated patients, cuff pressure measurement during insertion of a gastric tube is a new, simple and reliable bedside method to detect endotracheal malpositioning of a GT.     

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

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