Alveolar Dead Space Fraction Research Articles

Variáveis capnográficas pré e pós-tromboendarterectomias pulmonares

In these case report, the results of late dead space fraction (fDlate), end-tidal alveolar dead space fraction (AVDSf), arterial-alveolar gradient CO2 [P(a-et)CO2], and slope phase 3 of spirogram of two patients who underwent thromboendarterectomy for pulmonary embolism (PE) are shown. PE was diagnosed by pulmonary scintigraphy, helical tomography, and pulmonary angiography. The calculation of fDlate, AVDSf and P(a-et)CO2 was based on volumetric capnography associated with arterial blood gas analysis. The pre-operative fDlate of the first patient was 0.16 (cutoff 0.12) and AVDSf was 0.30 (cutoff 0.15). However, the fDlate of the second patient was false-negative (0.01) but, the AVDSf was positive (0.28). Postoperative fDlate of the first patient was -0.04 and AVDSf was 0.16; for the second patient, the values were 0.07 and 0.28, respectively. The association of these capnographic variables with image exams reinforces the importance of this noninvasive diagnosis method.

Cardiopulmonary effects of dexmedetomidine in goats and sheep anaesthetised with sevoflurane

In sheep, α2-agonists can induce severe hypoxaemia. In goats, reports on changes in oxygenation are inconsistent. The aim of this study was to compare the cardiopulmonary effects of dexmedetomidine in...

The Bedside Investigation of Pulmonary Embolism Diagnosis Study

We sought to determine whether using combinations of 3 bedside tests (7-variable clinical model, non-enzyme-linked immunosorbent assay D-dimer test, and alveolar dead-space fraction) to exclude pulmonary embolism (PE) before diagnostic imaging was as safe as a standard strategy of starting with ventilation-perfusion (V/Q) scan. In this double-blind, randomized, controlled equivalency trial, patients were randomized to initial bedside tests or to initial V/Q scan without bedside tests. Patients assigned to the bedside test group had a sham V/Q scan performed if at least 2 of 3 bedside test results were negative; otherwise, they underwent an actual V/Q scan. Further diagnostic management was determined by a blinded physician after V/Q scan. The primary outcome measure was recurrent venous thromboembolic events during 3 months among patients who were not taking anticoagulant agents after the initial investigations were completed. Four hundred fifty-eight consecutive adults with suspected PE were eligible for the study; 398 of 399 consenting and randomized patients completed the study. The follow-up venous thromboembolic event rate was 2.4% in the bedside test group vs 3.0% in the V/Q scan group (P = .76). Pulmonary embolism was excluded in 34% (67/199) of the bedside test group patients with at least 2 negative results on 3 bedside tests vs 18% (35/199) excluded using only the 7-variable clinical model and the D-dimer test. Excluding PE with at least 2 negative results on 3 bedside tests safely eliminates the need for diagnostic imaging in 34% of patients with suspected PE.

Estimating alveolar dead space from the arterial to end-tidal CO(2) gradient: a modeling analysis.

Using an original, validated, high-fidelity model of pulmonary physiology, we compared the arterial to end-tidal CO(2) gradient divided by the arterial CO(2) tension (Pa-E'CO(2)/PaCO(2)) with alveolar dead space expressed as a fraction of alveolar tidal volume, calculated in the conventional manner using Fowler's technique and the Bohr equation: (VDalv/VTalv)(Bohr-Fowler). We examined the variability of Pa-E'CO(2)/PaCO(2) and of (VDalv/VTalv)(Bohr-Fowler) in the presence of three ventilation-perfusion defects while varying CO(2) production (Vdot;CO(2)), venous admixture, and anatomical dead space fraction (VDanat). Pa-E'CO(2)/PaCO(2) was approximately 59.5% of (VDalv/VTalv)(Bohr-Fowler). During constant alveolar configuration, the factors examined (Vdot;CO(2), pulmonary shunt fraction, and VDanat) each caused variation in (VDalv/VTalv)(Bohr-Fowler) and in Pa-E'CO(2)/PaCO(2). Induced variation was slightly larger for Pa-E'CO(2)/PaCO(2) during changes in VDanat, but was similar during variation of venous admixture and Vdot;CO(2). Pa-E'CO(2)/PaCO(2) may be a useful serial measurement in the critically ill patient because all the necessary data are easily obtained and calculation is significantly simpler than for (VDalv/VTalv)(Bohr-Fowler). Using an original, validated, high-fidelity model of pulmonary physiology, we have demonstrated that the arterial to end-tidal carbon dioxide pressure gradient may be used to robustly and accurately quantify alveolar dead space. After clinical validation, its use could replace that of conventionally calculated alveolar dead space fraction, particularly in the critically ill.

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat.

Our objective was to test the effect of inhibition of thromboxane synthase versus inhibition of cyclooxygenase (COX)-1/2 on pulmonary gas exchange and heart function during simulated pulmonary embolism (PE) in the rat. PE was induced in rats via intrajugular injection of polystyrene microspheres (25 micro m). Rats were randomized to one of three posttreatments: 1) placebo (saline), 2) thromboxane synthase inhibition (furegrelate sodium), or 3) COX-1/2 inhibition (ketorolac tromethamine). Control rats received no PE. Compared with controls, placebo rats had increased thromboxane B(2) (TxB(2)) in bronchoalveolar lavage fluid and increased urinary dinor TxB(2). Furegrelate and ketorolac treatments reduced TxB(2) and dinor TxB(2) to control levels or lower. Both treatments significantly decreased the alveolar dead space fraction, but neither treatment altered arterial oxygenation compared with placebo. Ketorolac increased in vivo mean arterial pressure and ex vivo left ventricular pressure (LVP) and right ventricular pressure (RVP). Furegrelate improved RVP but not LVP. Experimental PE increased lung and systemic production of TxB(2). Inhibition at the COX-1/2 enzyme was equally as effective as inhibition of thromboxane synthase at reducing alveolar dead space and improving heart function after PE.

End tidal CO 2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism

Background: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO 2 (etCO 2) and tested two hypotheses: (1) that etCO 2 can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO 2 during resuscitation to a greater extent than arrhythmic cardiac arrest. Methods: Anesthetized, mechanically ventilated rats ( N=10 per group), were subjected to either graded PE (latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. Results: At a MAP of 40 mmHg, etCO 2 was significantly decreased in the PE group (18.3±1.9 torr) compared with both the hemorrhage (24.3±1.3) and the control group (35.0±1.3 torr; ANOVA P<0.001). The decreased etCO 2 occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO 2 was significantly decreased in the PE group (6.5±0.9) versus both hemorrhage (16.5±1.1) and TTX (34.2±2.4 torr). Conclusions: Massive PE with shock decreases the etCO 2 and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO 2 readings during CPR.

A normal alveolar dead space fraction plus d-dimer assay ruled out suspected pulmonary embolism in the emergency department

(2001) JAMA 285, 761; Kline JA, Israel EG, Michelson EA, et al. . Diagnostic accuracy of a bedside . d . -dimer assay and alveolar dead-space measurement for rapid exclusion...

A normal alveolar dead-space fraction plus D-dimer assay ruled out suspected pulmonary embolism in the emergency department

Source Citation Kline JA, Israel EG, Michelson EA, et al. Diagnostic accuracy of a bedside D-dimer assay and alveolar dead-space measurement for rapid exclusion of pulmonary embolism: a multicenter study. JAMA. 2001 Feb 14;285:761-8. 11176914

Steady-State End-Tidal Alveolar Dead Space Fraction and D-Dimer: Bedside Tests To Exclude Pulmonary Embolism

Less than 35% of patients suspected of having pulmonary embolism (PE) actually have PE. Safe bedside methods to exclude PE could save health-care resources and improve access to diagnostic testing for suspected PE. In patients with suspected PE, we sought to determine the sensitivity, specificity, and negative predictive value of (1) a steady-state end-tidal alveolar dead space fraction (AVDSf) of < 0.15, (2) a negative D-dimer result, and (3) the combination of a steady-state end-tidal AVDSf of < 0.15 and a negative D-dimer result. Prospective cohort study. Tertiary-care center in Ottawa, Ontario, Canada. Consecutive inpatients, outpatients, and emergency department patients with suspected PE referred to the Departments of Nuclear Medicine or Radiology for investigation of suspected PE. All study patients had D-Dimer and alveolar dead space measurements prior to determining outcome (PE or no PE) with ventilation/perfusion scans and/or noninvasive leg vein imaging and/or pulmonary angiography. Two hundred forty-six eligible and consenting patients underwent diagnostic imaging that excluded PE in 163 patients, diagnosed PE in 49 patients, and was indeterminant in 34 patients. A negative D-dimer result excluded PE with a sensitivity of 83.0% (95% confidence interval [CI], 69.2 to 92.4%), a negative predictive value of 91.2% (95% CI, 83.4 to 96.1%), and a specificity of 57.6%. A steady-state end-tidal AVDSf of < 0.15 excluded PE with a sensitivity of 79.5% (95% CI, 63.5 to 90.7%), a negative predictive value of 90.7% (95% CI, 82.5 to 95.9%), and a specificity of 70.3%. The combination of a negative D-dimer result and a steady-state end-tidal AVDSf of < 0.15 excluded PE with a sensitivity of 97.8% (95% CI, 88.5 to 99.9%), a negative predictive value of 98.0% (95% CI, 89.4 to 99.9%), and a specificity of 38.0%. This simple combination of bedside tests may safely rule out PE without further diagnostic testing in large numbers of patients with suspected PE.

Pressure-controlled inverse ratio ventilation after cardiac surgery

Background and objective Pressure-controlled inverse ratio ventilation was compared with controlled mechanical ventilation in patients after cardiac surgery. Methods Ten patients were ventilated after sternal closure using a Siemens Servo 900C ventilator to a target end-tidal PCO2 of 4.0 kPa. They were randomized to receive controlled mechanical ventilation or pressure-controlled inverse ratio ventilation. CO2-based data were recorded on a laptop personal computer, which together with arterial PCO2 permitted measurement of the respiratory dead space. Once measurements were complete the ventilator was switched to the other mode and new measurements taken. Results PaCO2 and CO2 were virtually the same in both modes. Peak airway pressure (17.2 ± 2.7 vs. 20.8 ± 2.5 cmH2O, P < 0.01) and minute ventilation (4.9 ± 1.1 vs. 5.3 ± 1.1 cmH2O, P < 0.01) were less during pressure-controlled inverse ratio ventilation. Physiological dead space fraction (0.39 ± 0.06 vs. 0.51 ± 0.05, P < 0.001), airway dead space (56 ± 15 vs. 81 ± 15 mL, P < 0.001) and alveolar dead space fraction (0.25 ± 0.07 vs. 0.31 ± 0.09, P < 0.01) were all less during pressure-controlled inverse ratio ventilation. There were no differences in heart rate or mean arterial pressure. Conclusions The prolonged inspiratory period and pressure-controlled flow pattern of pressure-controlled inverse ratio ventilation reduce the alveolar and airway dead spaces, and give lower peak airway pressures, compared with conventional ventilation, in cardiac surgical patients.

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.

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)

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.

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).

Changes in the arterial to end‐tidal Pco2 differences during coronary artery bypass grafting

The arterial to end-tidal PCO2 difference, PaCO2-PE,CO2, was measured at four different stages during coronary artery bypass grafting in 43 patients: 1) before sternotomy; 2) after sternotomy, sternum retracted; 3) after bypass, sternum still retracted; 4) sternum closed. Mean PaCO2-PE,CO2 initially was 0.6 kPa and changed scarcely at all during the procedure. There were, however, some moderate individual changes in PaCO2-PE,CO2 during surgery, the range of changes compared to the initial value being from -1.4 to +1.3 kPa. The standard deviations for the changes from stage to stage were 0.3-0.4 kPa. PaCO2-PE,CO2 changed by more than 0.5 kPa on only 12 occasions in ten patients. The limitations of PaCO2-PE,CO2 as an index of the alveolar deadspace fraction and the efficiency of ventilation are discussed.

RELATIONSHIP BETWEEN ALVEOLAR DEADSPACE AND ARTERIAL OXYGENATION IN CHILDREN WITH CONGENITAL CARDIAC DISEASE

Fifty-eight children were studied during nitrous oxide in oxygen and fentanyl anaesthesia before undergoing closed or open cardiac surgery. FlO2 was 0.5. Alveolar deadspace was measured using the carbon dioxide single breath test (SBT-CO2) obtained from a computerized online system for monitoring expired CO2 and airway flow, based on the Servo ventilator, Arterial blood was sampled simultaneously for measurement of PaCO2 and PaO2. There was a marked reciprocal relationship between PaO2 and the alveolar deadspace fraction. In children with a normal pulmonary circulation and good oxygenation, alveolar deadspace fraction was approx. 0.05. Shunts which reduced PaO2 to 10 kPa produced a deadspace fraction of 0.15. When PaO2 was 3-4 kPa, alveolar deadspace fraction was approx. 0.4. In well-oxygenated children, alveolar deadspace fraction was only slightly greater than predicted by a model of the effects of pure right-to-left shunting. In severely cyanotic children, the discrepancy between predicted and observed VDalv/VTalv was greater. The mean arterial-end-tidal CO2 difference was zero in children in whom PaO2 was greater than 10 kPa, despite a measurable alveolar deadspace. In severely hypoxic children, the difference was 1-2 kPa. In a retrospective analysis of published data from anaesthetized adults without intracardiac shunting, no relationship was found between alveolar deadspace and PaO2.

Noninvasive measurement of cardiac output using partial CO2 rebreathing.

A noninvasive algorithm for estimating cardiac output is discussed. The technique is based on a differential form of the CO/sub 2/ Fick equation applied during normal ventilation and a 30-s period of partial rebreathing using additional deadspace. Using the Fick equation in a differential form eliminates the need to estimate mixed venous pCO/sub 2/, also the sensitivity of the cardiac output estimate to changes in the alveolar deadspace fraction is greatly reduced. The procedure is fully automated, requires minimal staff supervision, and provides cardiac output estimates every 3 1/2-min. Estimates of cardiac output when compared to thermodilution yielded a correlation coefficient of 0.92 with a linear regression slope of 0.92 (n=451). Temporary increases in alveolar deadspace did not significantly alter this relationship. Cardiac output estimates obtained during period of increased pulmonary shunt due to oleic acid infusion yielded a correlation coefficient of 0.90 with a linear regression slope of 0.92 when compared to direct thermodilution measurements. >

Gas exchange during thoracotomy in children. A study using the single-breath test for CO2.

Gas exchange during thoracotomy was studied in 13 children aged 6 months to 14 years (median age 5 years), anaesthetized for repair of coarctation of the aorta or closure of a patent ductus arteriosus. All received halothane in equal parts of N2O/O2 supplemented with fentanyl. CO2 single-breath tests were obtained with a computerised on-line system based on the Servo ventilator. From signals for airway flow pressure, CO2 concentration and timing, the computer calculated the airway deadspace (VDaw) and the static compliance and resistance of the respiratory system. Given a value for PaCO2, the computer also calculated the physiological and alveolar deadspaces. Measurements were taken at six stages during the procedure, starting with the supine position before surgery. After turning to the lateral position, airway deadspace increased by 19%, thus increasing the physiological deadspace fraction. When the pleura was opened, both VDaw and PaO2 were reduced. When the upper lung was retracted, compliance was reduced and also PaO2 - the minimum value noted was 17.3 kPa. Hypoxic PaO2 values were possibly avoided because both ventilation and perfusion were reduced in the retracted lung. The alveolar deadspace fraction increased during these intra-operative stages. Although the net effect of the changes in airway and alveolar deadspace during surgery was a significant increase in physiological deadspace fraction (from 0.23 to 0.28), gas exchange could be maintained at the cost of only moderate increases in peak airway pressure: the mean increase was from 2.4 to 2.8 kPa (24 to 29 cmH2O).(ABSTRACT TRUNCATED AT 250 WORDS)

Increased alveolar deadspace after closure of cardiac septal defects: pulmonary air embolism or failure of homeostasis?

During surgery for closure of atrial or ventricular septal defects (ASD, VSD), we used a computerized on-line system to follow changes in the alveolar deadspace fraction. We observed a large increase in the alveolar deadspace immediately following septal defect closure. No increase had been observed post-cardio-pulmonary bypass in children operated upon because of aortic or pulmonary stenosis, or in adults undergoing myocardial revascularization. The increase in deadspace is probably a result of the lung's failure to adjust to the large decrease in pulmonary blood flow following septal defect closure. An alternative cause for the finding, that of pulmonary artery air embolism occurring intraoperatively, appears to be less likely.