Dead Space Fraction Research Articles

Impact of Different Inspiratory Flow Patterns on Arterial CO2-tension

Ventilation with decelerating inspiratory flow is known to reduce the dead space fraction and to decrease PaCO2. Constant inspiratory flow with an end-inspiratory pause (EIP) is also known to increase the removal of CO2.The aim of the study was to elucidate the effect of the pause/no-flow period while both the pattern and rate of inspiratory flow was unchanged, and when the lung was ventilated with sufficient PEEP to prevent end-expiratory collapse.Surfactant depleted piglets were assigned to decelerating or constant inspiratory flow with 24 breaths per minute (bpm) or 12 bpm, or to constant flow, without and with an end-inspiratory pause of 25%. By adding an EIP the total time without active inspiratory flow of the respiratory cycle was kept unchanged. Gas exchange, airway pressures, functional residual capacity (using sulfurhexafluoride) and haemodynamics (thermo-dye indicator dilution technique) were measured.Irrespective of ventilatory frequency, PaCO2 was lower and serial dead space reduced with decelerating flow, compared with constant inspiratory flow. With an end-inspiratory pause added to constant inspiratory flow, serial dead space was reduced but did not decrease PaCO2.The results of this study corroborate the assumption that total time without active inspiratory flow is important for arterial CO2-tension.

Bedside noninvasive detection of acute pulmonary embolism in critically ill surgical patients.

We hypothesized that late pulmonary dead space fraction (Fd(late)) would be a useful tool to screen for pulmonary embolism (PE) in a group of surgical patients, including patients who required mechanical ventilation and patients with adult respiratory distress syndrome. We prospectively calculated Fd(late) in patients with suspected PE who underwent pulmonary angiography. University-based, level I trauma center. Ability of Fd(late) to identify patients with PE. Twelve patients had 14 angiograms for suspected PE. The Fd(late) was 0.12 or above in all 5 patients who had PE; 4 required mechanical ventilation. The Fd(late) values were below 0.12 in 8 of 9 patients without PE. Four patients had adult respiratory distress syndrome. The Fd(late) had 100% sensitivity and 89% specificity for the detection of PE. The Fd(late) is a valuable tool for bedside screening of PE in surgical patients. We were able to accurately detect all PEs.

Pulmonary gas exchange during intramedullary fixation of femoral shaft fractures.

This study was undertaken to determine if the alveolar dead space fraction (Vd/Vt) or the alveolar-arterial oxygen gradient (A-a DO2) increased during intramedullary fixation of femoral shaft fractures. Fifty hemodynamically stable patients with femur fractures were prospectively enrolled. Three serial measurements of Vd/Vt and A-a DO2 were obtained immediately before femoral nailing (Pre), 30 minutes after nailing (+30), and 120 minutes after nailing (+120). Vd/Vt was determined by simultaneously measuring PaCO2 and the steady-state end-tidal CO2 (PetCO2), where Vd/Vt = (1 - PetCO2/PaCO2). Vd/Vt before nailing was 0.09 +/- 0.09 (mean +/- SD); at +30 and +120, Vd/Vt was 0.10 +/- 0.06 and 0.08 +/- 0.07, respectively (p > 0.2; paired t test, both time points). A-a DO2 before nailing was 84 +/- 85 mm Hg, and it did not change significantly at +30 (89 +/- 69 mm Hg; p = 0.51 vs. Pre; paired t-test) or at +120 (51 +/- 45 mm Hg). No difference in data was found with analysis by fracture classification or number of reamer passes. Vd/Vt and A-a DO2, however, were both significantly increased in patients with lung contusion (n = 6) before nailing, but neither measurement increased after nailing. One patient developed fat embolism (Vd/Vt of 0.35 at Pre and 0.31 at +120), and another patient experienced postoperative pulmonary thromboembolism (Vd/Vt increased from 0.06 at Pre to 0.17 at +120). The process of femoral nailing does not cause enough pulmonary embolization to alter pulmonary gas exchange as measured by Vd/Vt and A-a DO2. If Vd/Vt is increased preoperatively, the likelihood of subsequent pulmonary dysfunction secondary to either preoperative lung injury or fat embolism is increased.

Clinical assessment of gas exchange in mature horses.

There are limited methods of assessing pulmonary function in horses at rest. We developed clinical techniques to measure gas exchange efficiency in horses and evaluated 3 groups of horses that were 1) asymptomatic based on auscultation with rebreathing, transtracheal aspirate cytology, and thoracic radiographs (n = 6), 2) asymptomatic at rest but symptomatic with rebreathing (n = 11) and 3) symptomatic at rest (n = 9). Blood samples were obtained from the transverse facial artery and jugular vein. Maximal end-tidal CO2 tension (PETCO2) was measured by an infrared capnograph through a facemask. Alveolar O2 tension, dead space fraction (V(D)/V(T)), and physiological shunt fraction (Q(S)/Q(T)) were calculated using standard formulae. Arterial O2 tension in Group 1 horses (mean +/-s.d.103+/-3 mmHg) was significantly higher than in Group 2 or Group 3 horses. Q(S)/Q(T) in Group 1 horses (0.37+/-0.98%) was significantly lower than in Group 2 and Group 3 horses. Mean +/-s.d.V(D)/V(T) in Group 1 horses (-18.2+/-3.1) was significantly lower than Group 3 horses but not Group 2 horses.

A physiology simulator: validation of its respiratory components and its ability to predict the patient's response to changes in mechanical ventilation

We aimed to validate the mathematical validity and accuracy of the respiratory components of the Nottingham Physiology Simulator (NPS), a computer simulation of physiological models. Subsequently, we aimed to assess the accuracy of the NPS in predicting the effects of a change in mechanical ventilation on patient arterial blood-gas tensions. The NPS was supplied with the following measured or calculated values from patients receiving intensive therapy: pulmonary shunt and physiological deadspace fractions, oxygen consumption, respiratory quotient, cardiac output, inspired oxygen fraction, expired minute volume, haemoglobin concentration, temperature and arterial base excess. Values calculated by the NPS for arterial oxygen tension and saturation (PaO2 and SaO2), mixed venous oxygen tension and saturation (PvO2 and SvO2), arterial and mixed venous carbon dioxide tension (PaCO2 and PvCO2) and arterial pH were accurate compared with measured values. Subsequently, arterial gas responses to changes in minute volume of FiO2 were measured in 31 patients and were compared with the NPS prediction for each response. The 95% limits of agreement in predicting the magnitude of change were: arterial oxygen tension -2.07 to 2.47 kPa; PaCO2 -0.33 to 0.67 kPa; and pH -0.023 to 0.033. This investigation has validated respiratory components of the NPS. We recommend the NPS as a clinical tool for predicting the effects of alterations in mechanical ventilation in stable patients in the intensive care unit.

Equipment review: Tracheal gas insufflation

Tracheal gas insufflation (TGI) is an adjunctive ventilatory technique that delivers fresh gas into the trachea either continuosly or only during a specific segment of the respiratory cycle (phasic flow) [1,2,3,4]. Two mechanisms are responsible for improving the efficacy of conventional tidal breaths during TGI [5,6,7]. First, fresh gas introduced by the catheter during expiration flushes the series (anatomic) deadspace compartment proximal to its tip free of CO2. Consequently, during the subsequent inspiration, less CO2 is recycled back to the alveoli thus improving CO2 elimination. Second, at high catheter flow rates, turbulence generated at the tip of the catheter can enhance gas mixing in regions distal to the catheter tip, thereby contributing to CO2 removal. Carbon dioxide elimination during TGI depends on catheter flow rate because fresh gas flushes a greater portion of the proximal deadspace at higher flow rates. Moreover, at higher flow rates, turbulence generated at the catheter tip may further enhance distal gas mixing. The volume of fresh gas introduced into the trachea during TGI depends on expiratory time (TE) and catheter flow rate (Vc). At a certain TE × Vc, fresh gas completely sweeps the proximal anatomic deadspace during expiration. At that point, increasing Vc most likely does not dilute the CO2 residing in the series deadspace any further. This operational charactertistic of TGI, and the fact that the decrease in the partial pressure of CO2 (PaCO2) caused by a reduction in total physiologic deadspace fraction (VD/VT) is much less at lower VD/VT, limits the decrement in PaCO2 afforded by TGI at high Vc [8]. Nevertheless, at high Vc (< 10–15 1/min) PaCO2 continues to decrease with increasing Vc, but at a slower rate [8,9,10]. Once the series deadspace is flushed completely by the fresh gas during expiration, the flow dependence of PaCO2 is thought to be secondary to enhanced turbulent mixing in the airways distal to the catheter tip [5,11,12]. TGI is unlikely to be very effective when the alveolar as opposed to the series compartment dominates the total physiologic deadspace; yet, at small tidal volumes (whenever series deadspace is especially high) or when alveolar ventilation is very low. TGI should be a helpful adjunct to conventional mechanical ventilation (CMV) [8].

The Effect of Volume Infusion on Dead Space in Mechanically Ventilated Patients With Severe Asthma

Mechanical ventilation of patients with severe asthma is associated with elevated airway pressures that may contribute to increased physiologic dead space. To our knowledge, no previous reports have considered the effect of intravascular volume status on dead space fraction. We herein describe three patients whose dead space decreased by a mean of 4.2% in response to intravascular volume expansion with 250 or 500 mL of normal saline solution administered as part of their routine treatment. No significant changes in CO2 production, minute volume, or airway pressures occurred over the time interval. We conclude with a brief discussion of potential mechanisms to explain these findings and their potential clinical application.

Adjunctive ventilatory measures in the critically injured patient

Adjunctive ventilatory strategies have been developed to improve oxygenation or CO2 removal during mechanical ventilation of critically ill patients. These techniques allow the clinician to attain clinical goals at lower levels of ventilatory support. These innovative techniques accomplish gas exchange external to the lungs (extracorporeal and intravenacaval gas exchange), augment alveolar ventilation by decreasing the physiologic dead space fraction of each tidal breath (tracheal gas insufflation), or administer therapeutic agents designed to improve the ventilation-perfusion matching of the lung (nitric oxide, surfactant replacement therapy, perflu-orocarbon-associated gas exchange, and prone positioning). At the current state of development, each of these adjuncts is promising. However, most lack solid clinical data defining their role in the care of critically ill patients.

Tracheal gas insufflation (TGI) in patients with increased deadspace fraction:the effect and its determining factors

Tracheal gas insufflation (TGI) in patients with increased deadspace fraction:the effect and its determining factors

Carbon dioxide elimination measures resolution of experimental pulmonary embolus in dogs.

Patients with severe pulmonary embolism can suffer progressive hypercapnia refractory to supramaximal mechanical ventilation, and may require open-thoracic or transvenous emergency embolectomy in addition to anticoagulation and/or thrombolysis. The functional recovery of gas exchange would be signaled by an increase in pulmonary CO2 elimination and decrease in CO2 retention; such data could guide the course of operative embolectomy. Accordingly, we studied five chloralose-urethane anesthetized, mechanically ventilated dogs with open thoraces in which the right pulmonary arteries (RPAs) were reversibly occluded with cloth snares. After waiting for steady state, we abruptly released the snare to restore RPA perfusion and experimentally simulate resolution of pulmonary embolism. For 70 min we serially measure the CO2 volume exhaled per breath (VCO2,br), arterial, mixed venous, and end-tidal PCO2 (PACO2, PVCO2, PETCO2), cardiac output (QT), and the alveolar dead space fraction (VDalv/VTalv = [PaCO2 - PETCO2/PaCO2). RPA reperfusion caused VCO2,br to significantly and abruptly increase from 8.9 +/- 2.7 to 11.6 +/- 3.6 mL; 70 min later VCO2,br had returned to baseline. PaCO2 and PVCO2 steadily decreased during 70 min of RPA reperfusion. PETCO2 increased from 25 +/- 5 to 33 +/- 5 mm Hg immediately after RPA reperfusion, as VDalv/VTalv decreased from 54% +/- 10% to 32% +/- 12%, but PETCO2 was still significantly greater than baseline at 70 min of RPA reperfusion. QT did not significantly change. We conclude that intraoperative measurement of VCO2,br should immediately detect and follow the resolution of CO2 retention in the lung and peripheral tissues after RPA reperfusion. PETCO2 could not detect the decrease of VCO2,br back to baseline because PETCO2 does not measure exhaled volume or the PCO2 waveform.

Carbon Dioxide Elimination Measures Resolution of Experimental Pulmonary Embolus in Dogs

Patients with severe pulmonary embolism can suffer progressive hypercapnia refractory to supramaximal mechanical ventilation, and may require open-thoracic or transvenous emergency embolectomy in addition to anticoagulation and/or thrombolysis. The functional recovery of gas exchange would be signaled by an increase in pulmonary CO2 elimination and decrease in CO2 retention; such data could guide the course of operative embolectomy. Accordingly, we studied five chloralose-urethane anesthetized, mechanically ventilated dogs with open thoraces in which the right pulmonary arteries (RPAs) were reversibly occluded with cloth snares. After waiting for steady state, we abruptly released the snare to restore RPA perfusion and experimentally simulate resolution of pulmonary embolism. For 70 min we serially measure the CO (2) volume exhaled per breath (VCO2,br), arterial, mixed venous, and end-tidal PCO2 (PaCO2, PVCO2, PETCO2), cardiac output (QT), and the alveolar dead space fraction (VDalv/VTalv = [PaCO2 - PETCO2]/PaCO2). RPA reperfusion caused VCO2,br to significantly and abruptly increase from 8.9 +/- 2.7 to 11.6 +/- 3.6 mL; 70 min later VCO2,br had returned to baseline. PaCO2 and PVCO2 steadily decreased during 70 min of RPA reperfusion. PETCO (2) increased from 25 +/- 5 to 33 +/- 5 mm Hg immediately after RPA reperfusion, as VDalv/VTalv decreased from 54% +/- 10% to 32% +/- 12%, but PETCO2 was still significantly greater than baseline at 70 min of RPA reperfusion. QT did not significantly change. We conclude that intraoperative measurement of VCO (2),br should immediately detect and follow the resolution of CO2 retention in the lung and peripheral tissues after RPA reperfusion. PETCO2 could not detect the decrease of VCO2,br back to baseline because PETCO2 does not measure exhaled volume or the PCO2 waveform. (Anesth Analg 1996;83:247-53)

The Effect of Laparoscopic Cholecystectomy on Cardiovascular Function and Pulmonary Gas Exchange

Hemodynamic changes, pulmonary CO2 elimination (VECO2) and gas exchange were evaluated during laparoscopic cholecystectomy.An algorithm to calculate inspired ventilation (VI) needed to maintain constant PaCO2 was also developed. In 12 ASA physical status I patients undergoing laparoscopic cholecystectomy, heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI) were measured by the analysis of a radial artery pressure profile before, during, and after CO2 insufflation. Alveolar-arterial oxygen pressure gradient (P(A-a)O2), physiological and alveolar ventilatory dead space fractions (VDphys/VT; VDalv/VT), and PaCO2 were measured as well. VECO2 was assessed every minute in the patients maintained in the head-up position. HR did not significantly change during pneumoperitoneum, whereas MAP showed a transient increase (24.9%; P < 0.05) after CO2 insufflation. CI remained stable during pneumoperitoneum, but increased (25.0%; P < 0.05) after deflation. As a consequence, SVRI transiently increased after CO2 insufflation and decreased by 15.8% (P < 0.05) 5 min after deflation. P(A-a)O (2) increased slightly (P < 0.05) with increased anesthesia time. VDphys/VT and VDalv/VT did not change after pneumoperitoneum onset, but VDalv/VT decreased after CO2 deflation (13.4%; P < 0.05). VECO2 increased (decreased) after a monoexponential time course during (after) CO2 insufflation in 8 of 12 patients. The mean time constants (t) of the monoexponential functions were 26.3 and 15.4 min during and after pneumoperitoneum. A monoexponential time course was shown also by PaCO2 during CO2 insufflation (tau = 27.8 min). Finally, the VI needed to maintain PaCO2 at a selected value could be calculated by the following algorithm: VI = [0.448 centered dot (1 - e-t/tau) + 2.52] centered dot (VA centered dot PaCO (2) centered dot 713)-1, where VA corresponds to alveolar ventilation and t must be chosen according to the pneumoperitoneum phase. We conclude that CO2 insufflation in the abdominal cavity does not induce significant changes in cardiopulmonary function in ASA physical status I patients. The algorithm proposed seems to be a useful tool for the anesthesiologists to maintain constant PaCO2 during all surgical procedures. (Anesth Analg 1996;83:134-40)

The effect of laparoscopic cholecystectomy on cardiovascular function and pulmonary gas exchange.

Hemodynamic changes, pulmonary CO2 elimination (VECO2) and gas exchange were evaluated during laparoscopic cholecystectomy. An algorithm to calculate inspired ventilation (VI) needed to maintain constant PaCO2 was also developed. In 12 ASA physical status I patients undergoing laparoscopic cholecystectomy, heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI) were measured by the analysis of a radial artery pressure profile before, during, and after CO2 insufflation. Alveolar-arterial oxygen pressure gradient (P(A-a)O2), physiological and alveolar ventilatory dead space fractions (VDphys/VT; VDalv/VT), and PaCO2 were measured as well. VECO2 was assessed every minute in the patients maintained in the head-up position. HR did not significantly change during pneumoperitoneum, whereas MAP showed a transient increase (24.9%; P < 0.05) after CO2 insufflation. CI remained stable during pneumoperitoneum, but increased (25.0%; P < 0.05) after deflation. As a consequence, SVRI transiently increased after CO2 insufflation and decreased by 15.8% (P < 0.05) 5 min after deflation. P(A-a)O2 increased slightly (P < 0.05) with increased anesthesia time. VDphys/VT and VDalv/VT did not change after pneumoperitoneum onset, but VDalv/VT decreased after CO2 deflation (13.4%; P < 0.05). VECO2 increased (decreased) after a monoexponential time course during (after) CO2 insufflation in 8 of 12 patients. The mean time constants (t) of the monoexponential functions were 26.3 and 15.4 min during and after pneumoperitoneum. A monoexponential time course was shown also by PaCO2 during CO2 insufflation (tau = 27.8 min). Finally, the VI needed to maintain PaCO2 at a selected value could be calculated by the following algorithm: VI = [0.448.(1-e(-t/tau) + 2.52].(VA.PaCO2.713)-1, where VA corresponds to alveolar ventilation and t must be chosen according to the pneumoperitoneum phase. We conclude that CO2 insufflation in the abdominal cavity does not induce significant changes in cardiopulmonary function in ASA physical status I patients. The algorithm proposed seems to be a useful tool for the anesthesiologists to maintain constant PaCO2 during all surgical procedures.

Respiratory variables during thoracotomy for PDA ligation.

Physiological deadspace fraction of tidal volume (VD/VT), arterial to end-tidal carbon dioxide tension differences [P(a-E')CO2], arterial oxygen tension (PaO2) and respiratory system compliance were studied in twenty patients with patent ductus ateriosus scheduled for multiple ligation and transfixation through posterolateral thoracotomy under general anaesthesia with controlled ventilation. The study period was divided into six stages: stage 1--supine posture under anaesthesia, stage 2--lateral posture before start of surgery, stage 3--after chest opening before lung manipulation, stage 4--after ductus ligation and lung re-expansion before chest closure, stage 5--lateral posture, chest closed, stage 6--supine stage before reversal. There was a significant (P < 0.01) increase of VD/VT on attaining the lateral posture. The fraction decreased significantly (P < 0.05) on opening of the chest (stage 3) and subsequently increased at stage 4. There was no significant change in mean P(a-E')CO2 at various stages of thoracotomy. PaO2 fell significantly on opening of the chest and was lowest before chest closure (stage 4). PaO2 increased following chest closure but was still significantly lower than the pre-surgical supine stage. Respiratory system compliance was lowest at stage 4. Changes in deadspace fraction VD/VT do not correspond favourably to arterial oxygen tensions during posterolateral thoractomy.

Clinical evaluation of diminished early expiratory flow (DEEF) ventilation in mechanically ventilated COPD patients

To evaluate the cardiopulmonary effects, especially the end-expiratory lung volume (EEV) and ventilation inhomogeneity during diminished early expiratory flow ventilation (DEEF), which resembles pursed-lips breathing, with the conventional intermitent positive pressure ventilation (IPPV) in postoperative mechanically ventilated patients with chronic obstructive pulmonary disease (COPD). A prospective study measuring cardiopulmonary parameters during IPPV, DEEF, and positive end-expiratory pressure (PEEP) as a control mode. In the PEEP mode, PEEP values were chosen such that the mean airway pressure during a breath cycle was equal to that during the DEEF mode, which was higher than the conventional IPPV mode. Surgical intensive care unit of a university hospital. 20 postoperative mechanically ventilated COPD patients who were optimally pretreated and had normal blood oxygenation. Measurements were started in the IPPV (IPPV1) mode, continued in a randomized order with DEEF or PEEP, and completed with a second IPPV (IPPV2) mode, with 1 h equilibration time in each mode before each measurement. A multi-breath indicator gas wash-out test was used to calculate the EEV and ventilation inhomogeneity. There was a 9% increase (p<0.05) in the mean EEV during both the DEEF and PEEP mode compared to IPPV. No significant changes in the ventilation inhomogeneity and deadspace fractions or the hemodynamic parameters were found during the different ventilatory modes. There was no improvement in pulmonary and hemodynamic parameters during the DEEF mode in comparison to the IPPV mode. The small increase in EEV during DEEF was probably caused by the slightly higher mean expiratory pressures as in the PEEP mode. However, this had no effect on the hemodynamic parameters. As we could not observe any improvement with the DEEF ventilation in our optimally pretreated postoperative COPD patients, we do not advise applying this therapy in this group of patients, since this mode of ventilation may cause barotrauma if not monitored adequately.

Comparison of end-tidal PCO2 and average alveolar expired PCO2 during positive end-expiratory pressure.

The measurement of average alveolar expired PCO2 (PAECO2) weights each PCO2 value on the alveolar plateau of the CO2 expirogram by the simultaneous change in exhaled volume. PAECO2 can be determined from a modified analysis of the Fowler anatomic dead space (VDANAT). In contrast, end-tidal PCO2 (PETCO2) only measures PCO2 in the last small volume of exhalate. In conditions such as mechanical ventilation with positive end-expiratory pressure (PEEP), where the alveolar plateau can have a significant positive slope, we questioned how much PETCO2 could overestimate PAECO2. Accordingly, in six anesthetized ventilated dogs, we digitally measured and processed tidal PCO2 and flow to determine VDANAT. We determined PETCO2 and PAECO before and after the application of 7.6 cm H2O PEEP. Alveolar dead space to tidal volume fraction (VD/VT) was determined by [arterial PCO2- alveolar PCO2]/arterial PCO2, where alveolar PCO2 was determined by either PETCO2 or PAECO2. During baseline ventilation, PETCO2 was 3.4 mm Hg (approximately 11%) greater than PAECO2. Because PEEP significantly increased the slope of the alveolar plateau from 28 to 74 mm Hg/L, the difference between PETCO2 and PAECO2 significantly increased to 6.6 mm Hg (approximately 20% difference). The concurrent increase in VDANAT during PEEP decreased alveolar tidal volume and tended to limit the overestimation of PETCO2 compared to PAECO2. When alveolar PCO2 was estimated by PETCO2, alveolar VD/VT was 18%, compared to an alveolar VD/VT of 26% when alveolar PCO2 was estimated by PAECO2. This difference was significantly magnified during PEEP ventilation. The overestimation of PAECO2 by PETCO2 can result in a falsely high assessment of overall alveolar PCO2. Moreover, the use of PETCO2 to estimate alveolar PCO2 in the determination of the alveolar dead space fraction can result in falsely low and even negative values of alveolar dead space.

Cardiopulmonary Effects of Positive Pressure Ventilation During Acute Lung Injury

To assess the gas exchange and hemodynamic effects of pressure-limited ventilation (PLV) strategies in acute lung injury (ALI). We hypothesized that in ALI, the reduction of plateau airway pressure (Paw) would be associated with less alveolar overdistention and thus have better hemodynamic and gas exchange characteristics than larger tidal volume (Vr) ventilation. Laboratory. Prospective time-controlled sequential animal study. Right atrial, pulmonary artery, left atrial, arterial, lateral pleural (Ppl), and pericardial (Ppc) pressures, Paw, ventricular stroke volume, mean expired CO2, and arterial and mixed venous oxygen contents. Airway resistance and static lung compliance were also measured. Intermittent positive pressure ventilation (IPPV) given before (control) and after induction of ALI by oleic acid infusion (0.1 mL/kg). IPPV at FIO2 of 1, VT of 12 mL/kg, and frequency adjusted to maintain normocarbia. ALI PLV was given during ALI and defined as that VT which gave a similar plateau Paw to that of control IPPV. High-frequency jet ventilation (HFJV) and ALI HFJV were also given and defined as frequency within 10% of heart rate and mean Paw similar to that during control IPPV. After ALI, static lung compliance, PaO2, and pH decreased, whereas airway resistance and PaCO2 increased. For a constant lung volume, Ppl and Ppc were not different between control and ALI. Both absolute dead space (VD) and intrapulmonary shunt fraction increased after ALI, but absolute VD was lower with ALI PLV and ALI HFJV when compared with ALI IPPV. Ventilation did not alter hemodynamics during ALI. Changes in lung volume determine Ppc and Ppl. PLV strategies do not alter hemodynamics but result in less of an increase in VD/VT than would be predicted from the obligatory decrease in VT.

Intrapulmonary gas mixing and dead space in artificially ventilated dogs.

In this study we have investigated the effects of breath holding and of the physical properties of gases on four different respiratory dead spaces (VD): the Fowler, the physiological, the washout and the inert gas dead space. The experiments were performed with dogs which were ventilated artificially with breathing patterns with different post-inspiratory breath holding times (ta) of 0, 0.5, 1.0 and 2.0 s. Tracer amounts of acetone, ether and enflurane were infused continuously into a peripheral vein and a bolus of a mixture of krypton, Freon12 and SF6 was introduced into the peritoneal cavity. After reaching steady state, samples of arterial blood, mixed venous blood and mixed expired air were taken simultaneously. From the partial pressures (Pa, PV and PE respectively) we determined the excretion (E = PE/PV), retention (R = Pa/PV) and the physiological dead space fraction (VD,phys/VT = (1- PE/Pa)) for each gas, where VT is tidal volume. Further, we recorded the expirograms of the six tracer gases and of CO2 from which the Fowler dead space fractions (VD,Fowler/VT) of the different gases were determined. Also the washout dead space fractions (VD,washout/VT) for He and SF6 were determined as well as the inert gas dead space fraction (VD,MIGET/VT) with the use of the multiple inert gas elimination technique (MIGET). With the exception of VD,phys/VT for SF6, all dead space fractions decreased with increasing ta. VD,phys/VT for the poorly soluble gas SF6 was considerably larger than VD,phys/VT for the remaining gases. For the highly soluble acetone VFowler/VT was considerably smaller than VD,Fowler/VT for the other gases. VD,washout,SF6/VT was always larger than VD,washout,He/VT and VD,Fowler,SF6/VT. Further, VD,phys/VT was larger than VD,Fowler/VT for SF6 and acetone. However, for gases with intermediate solubility in blood VD,phys/VT tended to be smaller than VD,Fowler/VT. We conclude that the respiratory dead spaces are affected by the breathing pattern and by the physical properties of gases, i.e. their diffusivity in alveolar gas and their solubility in blood or lung tissue.

Inspiratory tidal volume sparing effects of tracheal gas insufflation in dogs with oleic acid-induced lung injury

Purpose: Tracheal gas insufflation (TGI) improves the efficiency of conventional mechanical ventilation (CMV) by reducing the series dead space of the airways. Consequently, application of TO as an adjunct to CMV may permit reducing tidal volume (V t) while limiting CO 2 retention. We tested the extent to which panexpiratory TGI allows reduction of V t while maintaining Paco 2 constant in an oleic acid-induced lung injury model. Methods: We studied six anesthetized, paralyzed, and mechanically ventilated dogs. Oleic acid injury was induced by injecting 0.09 mL/kg of oleic acid into the right atrium. After stabilization of lung injury the V t-sparing effect of TO was tested by progressively increasing catheter flow rate (Vc) from 2 to 5, 10, and 15 L/min while decreasing V t by an amount that maintained Paco 2 constant (≈47 mm Hg) with respect to baseline (Vc = 0 L/ min). Results: Tidal volume was decreased from a baseline value of 0.360 ± 0.030 L to 0.238 ± 0.054 L at Vc of 15 L/min. The reduction in V t was associated with a decrement in peak and end-inspiratory plateau airway opening pressure from 32 ± 3 to 28 ± 6 cm H 2O and from 25 ± 2 to 21 ± 3 cm H 2O, respectively. Total physiological dead space fraction decreased from a baseline value of 0.60 ± 0.08 to 0.31 ± 0.20 during TGI at 15 L /min. TGI did not affect cardiac output, Pao 2, or pulmonary venous admixture. Conclusion: We conclude that TO can be a useful adjunct to CMV during acute lung injury to limit V t while avoiding CO 2 retention.

Intraoperative end-tidal carbon dioxide values and derived calculations correlated with outcome

To determine how much information concerning resuscitation and outcome is provided by the end-tidal CO2 and derived variables obtained during surgery. Retrospective chart review. Emergency hospital operating room. One hundred critically ill or injured patients requiring major surgery and having a mortality rate of 41%. Standard intraoperative monitoring, including continuous capnography, plus arterial blood gas analyses every 1 to 1.5 hrs during surgery. There was only a fair correlation between the PaCO2 and end-tidal CO2 (r2 = .14). The mortality rates in these patients were highest in those patients who had the lowest end-tidal CO2 values, the highest arterial to end-tidal CO2 differences, and the highest estimated alveolar deadspace fraction. A persistent end-tidal CO2 of < or = 28 torr (< or = 3.8 kPa) was associated with a mortality rate of 55% (vs. 17% in those patients with a higher end-tidal CO2). The mortality rate was also increased in patients with a persistent arterial to end-tidal CO2 difference of > or = 8 torr (> or = 1.1 kPa) (58% vs. 23%). End-tidal CO2 and derived values should be monitored closely in critically ill or injured patients. Efforts should be made--by increasing cardiac output and core temperature and by adjusting ventilation as needed--to maintain the end-tidal CO2 at > or = 29 torr (> or = 3.9 kPa) and the arterial to end-tidal CO2 difference at < or = 7 torr (< or = 1.0 kPa).