Re-inspiration of CO<Subscript>2</Subscript> from ventilator circuit: effects of circuit flushing and aspiration of dead space up to high respiratory rate

Introduction  

Dead space negatively influences carbon dioxide (CO₂) elimination, particularly at high respiratory rates (RR) used at low tidal volume ventilation in acute respiratory distress syndrome (ARDS). Aspiration of dead space (ASPIDS), a known method for dead space reduction, comprises two mechanisms activated during late expiration: aspiration of gas from the tip of the tracheal tube and gas injection through the inspiratory line - circuit flushing. The objective was to study the efficiency of circuit flushing alone and of ASPIDS at wide combinations of RR and tidal volume (V_T) in anaesthetized pigs. The hypothesis was tested that circuit flushing and ASPIDS are particularly efficient at high RR.     

Tracheal gas insufflation reduces the tidal volume while PaCO2 is maintained constant

Objective The aims of the present study were two-fold: first, to confirm the effect of tracheal gas insufflation (TGI) throughout the respiratory cycle on alveolar ventilation at various catheter flows and constant total inspired V_T as an adjunct to conventional volume cycled mechanical ventilation in patients with acute lung injury; second, to test the efficacy of TGI in the reduction of toal V_T, peak and mean airway pressure while maintaining PaCO₂ in its baseline value. The hemodynamic effect and the consequences on oxygenation as result of the reduction of V_T, were also estimated.Design Prospective study of patients with acute lung injury requiring mechanical ventilation.Setting: 12 bedded, adult polyvalent intensive care unit in a teaching hospital.Patients 7 paralyzed and sedated patients with acute respiratory failure were studied. All patients were clinically and hemodynamically stable without fluctuation of the body temperature. All patients were orally intubated with cuffed endotracheal tubes, and mechanically ventilated with a standard circuit of known compliance.Interventions Continuous flows (4 and 6 l/min) were delivered through a catheter positioned 1 cm above carina while tidal volume or PaCO₂ were maintained constant at their baseline value.Results In this study a modest level of TGI significantly enhanced CO₂ elimination in patients with acute respiratory failure. Improved ventilatory efficiency resulted from the functional reduction of dead space during TGI allowing the same PaCO₂ to be maintained at the same frequency with lower tidal volume and lower airway pressure requirement. Tidal volume, peak and mean airway pressure decreased linearly with catheter flow, without significant changes in oxygenation, while PaCO₂ remained stable.Conclusion The results of this study suggest that TGI may be an useful adjunct mode of mechanical ventilation that limits alveolar pressure and minute ventilation requirements.     

Computer simulation allows goal-oriented mechanical ventilation in acute respiratory distress syndrome

Introduction  

To prevent further lung damage in patients with acute respiratory distress syndrome (ARDS), it is important to avoid overdistension and cyclic opening and closing of atelectatic alveoli. Previous studies have demonstrated protective effects of using low tidal volume (V_T), moderate positive end-expiratory pressure and low airway pressure. Aspiration of dead space (ASPIDS) allows a reduction in V_T by eliminating dead space in the tracheal tube and tubing. We hypothesized that, by applying goal-orientated ventilation based on iterative computer simulation, V_T can be reduced at high respiratory rate and much further reduced during ASPIDS without compromising gas exchange or causing high airway pressure.     

Ventilation–perfusion inequality and carbon dioxide sensitivity in hypoxaemic chronic obstructive pulmonary disease (COPD) and effects of 6 months of long‐term oxygen treatment (LTOT)

The aim of our study was to find out how blood gas disturbances in stable, eucapnic, severe chronic obstructive pulmonary disease (COPD) patients with an arterial oxygen tension (PaO₂) value of 7·7 (6·1–8·4) kPa are affected by ventilation–perfusion (V_A/Q) relationships and carbon dioxide (CO₂) sensitivity and how these parameters are influenced by 6 months of long‐term oxygen treatment (LTOT). V_A/Q ratios were measured using the multiple inert gas elimination technique (MIGET). Mouth occlusion pressure 0·1 s after onset of inspiration (Pi0·1) and minute ventilation (V_E) were measured to assess respiratory drive response (ΔPi0·1/ΔPCO₂) and hypercapnic ventilatory response (HCVR) to CO₂ rebreathing. At the start of LTOT, a normal median respiratory drive response level of 1·2 (0·2–2·3) cm H₂O/kPa and a low median HCVR as compared with healthy individuals (P<0·001) were found. However, 7·9 (0–29·8)% of the V_E, was directed towards hypoperfused lung areas. The dispersion of ventilation (log SDV; 0·47–1·76), and the dispersion of perfusion (log SDQ; 0·66–1·07) were wider than normal. The PaO₂ level correlated inversely with mean V_A/Q ratio for ventilation (V mean) and shunt. The PaCO₂ level correlated inversely with HCVR and vital capacity. After 6 months of LTOT, no significant changes in daytime blood gas levels, CO₂‐sensitivity or V_A/Q ratios were found. V_E tended to be reduced by 1·0 l min^–1. Conclusions: An elevated V mean and probably shunting are important contributing factors for the reduced PaO₂ and hypercapnic ventilatory response is a major determinant of PaCO₂ in eucapnic stable hypoxaemic COPD. Six months of LTOT does not affect blood gases, CO₂ sensitivity or ventilation–perfusion relationships.     

Aspiration of dead space allows isocapnic low tidal volume ventilation in acute lung injury. Relationships to gas exchange and mechanics

OBJECTIVE: In acute lung injury (ALI) mechanical ventilation damages lungs. We hypothesised that aspiration and replacement of dead space during expiration (ASPIDS) allows normocapnic ventilation at higher end-expiratory pressure (PEEP) and reduced tidal volume (V(T)), peak and plateau pressures (Paw(peak), Paw(plat)), thus avoiding lung damage. SETTING: University Hospital. PATIENTS: Seven consecutive sedated and paralysed ALI patients were studied. Interventions and measurements: Single breath test for CO(2) and multiple elastic pressure volume (Pel/V) curves recorded from different end-expiratory pressures guided ventilatory setting at ASPIDS. ASPIDS was studied at respiratory rate (RR) of 14 min(-1) and then 20 min(-1) with minute ventilation maintaining stable CO(2) elimination. RESULTS: Alveolar and airway dead spaces were 24.3% and 31.3% of V(T), respectively. Multiple Pel/V curves showed a shift towards lower volume at decreasing PEEP, thus indicating that patients required a higher PEEP. At ASPIDS, PEEP was increased from 8.9 cmH(2)O to 12.6 cmH(2)O and VT reduced from 11 ml/kg to 8.9 ml/kg at RR 14 min(-1) and to 6.9 ml/kg at RR 20 min(-1). A significant decrease in Paw(peak) (36.7 vs 32 at RR 14 min(-1) and 28.7 at RR 20 min(-1)) and Paw(plat) (29.9 vs 27.3 at RR 14 min-1 and 24.1 at RR 20 min-1) were observed. PaCO(2) remained stable. No intrinsic PEEP developed. No side effects were noticed. CONCLUSIONS: ASPIDS allowed the use of higher PEEP at lower V(T) and inflation pressure and constant PaCO(2). Multiple Pel/V curves gave insight into the tendency of lungs to collapse.     

Aspiration of dead space in the management of chronic obstructive pulmonary disease patients with respiratory failure

INTRODUCTION: Carbon dioxide clearance can be improved by reducing respiratory dead space or by increasing the clearance of carbon-dioxide-laden expiratory gas from the dead space. Aspiration of dead space (ASPIDS) improves carbon dioxide clearance by suctioning out (during expiration) the carbon-dioxide-rich expiratory gas while replacing the suctioned-out gas with oxygenated gas. We hypothesized that ASPIDS would allow lower tidal volume and thus reduce exposure to potentially injurious airway pressures. METHODS: With 8 hemodynamically stable, normothermic, ventilated patients suffering severe chronic obstructive pulmonary disease we tested the dead-space-clearance effects of ASPIDS. We compared ASPIDS to phasic tracheal gas insufflation (PTGI) during conventional mechanical ventilation and during permissive hypercapnia, which was induced by decreasing tidal volume by 30%. The mean P(aCO(2)) reductions with PTGI flows of 4.0 and 6.0 L/min and during ASPIDS (at 4.0 L/min) were 32.7%, 51.8%, and 53.5%, respectively. Peak, plateau, and mean airway pressure during permissive hypercapnia were significantly lower than during conventional mechanical ventilation but PTGI increased peak, plateau, and mean airway pressure. However, pressures were decreased during permissive hypercapnia while applying ASPIDS. Intrinsic positive end-expiratory pressure also increased with PTGI, but ASPIDS had no obvious influence on intrinsic positive end-expiratory pressure. ASPIDS had no effect on cardiovascular status. CONCLUSIONS: ASPIDS is a simple adjunct to mechanical ventilation that can decrease P(aCO(2)) during conventional mechanical ventilation and permissive hypercapnia.     

Infectious and inflammatory dissemination are affected by ventilation strategy in rats with unilateral pneumonia

Objective To evaluate the effect of V_T reduction and alveolar recruitment on systemic and contralateral dissemination of bacteria and inflammation during right-side pneumonia.Design Interventional animal study.Setting University hospital research laboratory.Subjects A total of 54 male Wistar rats.Interventions One day after right lung instillation of 1.4×10⁷ Pseudomonas aeruginosa, rats were left unventilated or ventilated for 2 h at low V_T (6 ml/kg) with different strategies of alveolar recruitment: no PEEP, 8 cm H₂O PEEP, 8 cm H₂O PEEP in a left lateral position, 3 cm H₂O PEEP with partial liquid ventilation, or high V_T (set such as end-inspiratory pressure was 30 cm H₂O) without PEEP (ZEEP). After ventilation the lungs, spleen and liver were cultivated for bacterial counts. Global bacterial dissemination was scored considering the percentage of positive spleen, liver and left lung cultures. TNF- was assayed in plasma before and after mechanical ventilation.Measurements and results All rats had right-side pneumonia with similar bacterial counts. All mechanical ventilation strategies, with the exception of low V_T-PEEP 8, promoted contralateral lung dissemination. Overall bacterial dissemination was less in non-ventilated controls (22%) and low V_T-PEEP 8 (22%) than in high V_T-ZEEP (67%), low V_T-PEEP 8 in left lateral position (59%) and low V_T-ZEEP (56%) (p<0.05). Partial liquid ventilation prevented systemic bacterial translocation, but at the expense of contralateral bacterial seeding. Plasma TNF- concentration increased significantly after mechanical ventilation with no PEEP at both high and low V_T.Conclusions Our results suggest that PEEP might reduce the risk of ventilation-induced bacterial and inflammatory mediator dissemination during pneumonia.Electronic Supplementary Material Supplementary material is available in the online version of this article at http://dx.doi.org/10.1007/s00134-003-2147-7This study was supported by a grant from Fondation pour la Recherche Médicale.     

Multiple breath nitrogen dead space

Summary. Ventilatory efficiency for eliminating CO₂ is expressed by the physiological dead space, V_Dphys = (1-PE CO₂/Pa CO₂) ×V_T, where PE is the mixed exhaled and Pa the arterial CO₂-tension and V_T the tidal volume. We used data from the multiple breath N₂-wash-out with oxygen for calculating a functional dead space for nitrogen. V_DFN₂= (1 -FEN₂/FEN₂/FidN₂) ×V_T. F_EN₂ is the mixed exhaled N₂-fraction and FidN₂ the calculated mean alveolar N₂-fraction during a wash-out with the same number of breaths to reach 2% N₂ in end tidal air, but having completely even distribution. FidN₂ is shown to be 0·20±0·01 for wash-outs using 20–150 breaths. The method was applied to wash-outs from 21 healthy volunteers, 18 patients with chronic obstructive lung disease and two subjects with acute bronchospasm. V_DF was well related to V_D phys CO₂ (r= 0·78) but higher than the latter. In subjects with lung disease V_DF was inversely related to the degree of obstruction expressed by forced expiratory volume in one second per cent of vital capacity (r= 0·85). The subjects with bronchospasm had very high V_D/V_TMF, in relation to their FEV%. If airway dead space predicted from height and sex is subtracted from V_DF, the resulting alveolar dead space will be a good expression for uneven gas distribution in the lungs. We also deduced a direct mathematical relation between lung clearance index and V_D/V_TF. The documented good reproducibility of LCI is thus also valid for V_D/V_TF, while the latter better expresses ventilatory efficiency.     

Ineffective ventilation during exercise in patients with chronic congestive heart failure

Summary The pathophysiologic mechanisms causing exertional breathlessness in patients with chronic congestive heart failure (CHF) are not fully understood. Therefore, we have studied whether the ventilation in such patients is ineffective during exercise. Thirteen patients with treated chronic CHF (New York Heart Association class II-IV) and eight healthy controls underwent a maximal bicycle ergometer test with continuous analysis of expired air and frequent arterial blood sampling for gas and lactate analysis. All subjects were non-smokers and none had any signs of a pulmonary disease. Peak O₂ consumption of the patients was 14.9 ±5.3 ml min^-1 kg^-1 and that of controls 33.6 ±7.5 ml min^-1 kg^-1. In patients with CHF the ratio of pulmonary dead space to tidal volume was significantly elevated at peak exercise compared with that of the controls (0.36±0.08 vs. 0.20±0.07, P<0.05). The ventilatory equivalent for CO₂ (VE:VCO₂) was also significantly higher in patients than in controls during exercise (P<0.05). Furthermore, both the ventilatory equivalents for CO₂ and O₂ (VE:VD₂) had a significant inverse correlation with peak O₂ consumption (P<0.001 for VE:VT:O₂ and P<0.05 for VE:VO₂), O₂ consumption at anaerobic threshold (P<0.01) and O₂-pulse (P<0.001) among the patients. During exercise the arterial PO₂ and PCO₂ remained normal in patients and controls. These data indicate that in patients with chronic CHF wasted ventilation is pathologically increased during exercise, and this is related to the severity of the disease. Chronic CHF is not associated with decreased ventilatory reserve, hypoxaemia or alveolar hyperventilation. The ineffectiveness of ventilation is probably an important cause of exertional breathlessness in patients with CHF.     

The effect of induced hypothermia on respiratory parameters in mechanically ventilated patients

Aim

Mild hypothermia is increasingly applied in the intensive care unit. Knowledge on the effects of hypothermia on respiratory parameters during mechanical ventilation is limited. In this retrospective study, we describe the effect of hypothermia on gas exchange in patients cooled for 24 h after a cardiac arrest.

Methods

Respiratory parameters were derived from electronic patient files from 65 patients at the start and end of the hypothermic phase and at every centigrade increase in body temperature until normo-temperature, including tidal volume, positive end expiratory pressure (PEEP), plateau pressure, respiratory rate, exhaled CO₂ concentrations (etCO₂) and FIO₂. Static compliance was calculated as V_T/P_plateau − PEEP. Dead space ventilation was calculated as (PaCO₂ − etCO₂)/PaCO₂.

Results

During hypothermia, PaCO₂ decreased, at unchanged PaCO₂-etCO₂ gap and minute ventilation. During rewarming, PaCO₂ did not change, while etCO₂ increased at unchanged minute ventilation. Dead space ventilation did not change during hypothermia, but lowered during rewarming. During hypothermia, PaO₂/FIO₂ ratio increased at unchanged PEEP levels. Respiratory static compliance did not change during hypothermia, nor during rewarming.

Conclusion

Hypothermia possibly improves oxygenation and ventilation in mechanically ventilated patients. Results may accord with the hypothesis that reducing metabolism with applied hypothermia may be beneficial in patients with acute lung injury, in whom low minute ventilation results in severe hypercapnia.     

Influence of alveolar ventilation changes on calculated gastric intramucosal pH and gastric-arterial PCO2 difference

Objective: To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO₂ tension (PtCO₂), gastric arterial CO₂ tension difference (P_gapCO₂), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pH_gap). Design: Clinical prospective study. Setting: A medical intensive care unit in a university hospital. Patients: Ten critically ill, mechanically ventilated patients requiring hemodynamic monitoring with pulmonary artery catheter. Interventions: Gastric tonometer placement. A progressive increase in tidal volume (V_T) from 7 to 10 ml/kg followed by an abrupt return to baseline V_T level. Measurements and main results: Tonometer saline PtCO₂ and hemodynamic data were collected hourly at various V_T levels: H0 and H0' (baseline V_T = 7 ml/kg), H1 (V_T = 8 ml/kg), H2 (V_T = 9 ml/kg), H3 (V_T = 10 ml/kg), H4 (baseline V_T). During the “hyperventilation phase” (H0-H3), pHi (p < 0.01) and pH_gap (p < 0.05) increased but P_gapCO₂ remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the “hypoventilation phase” (H3-H4), pHi fell from 7.27 ± 0.11 to 7.23 ± 0.09 (p < 0.01) and P_gapCO₂ decreased from 16 ± 5 mmHg to 13 ± 4 mmHg (p < 0.05). V_T reduction was associated with a significant cardiac output elevation (p < 0.05). Conclusions: PaCO₂ and PtCO₂ are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the P_gapCO₂ is not affected by ventilation variations unless CO changes are associated. Received: 15 June 1998 Final revision received: 21 October 1998 Accepted: 16 November 1998     

Pulmonary clearance of inhaled [99Tcm]DTPA: effects of ventilation pattern

Summary. While a rise in lung volume is known to increase the pulmonary clearance of technetium-99m-labelled dietylene triamine pentaacetate ([⁹⁹Tc^m]DTPA), little interest has been focused on the effects of changes in ventilation frequency, tidal volume and airway pressure. We studied adult, anaesthetized and intubated rabbits during three ventilation patterns (VP) using pressure controlled ventilation (Servo Ventilator 900C). VP was either deep slow (f=20 min^-1, tidal volume (V_T) = 30 ± 4 ml kg^-1 and positive end-expiratory pressure (PEEP) = 0·2 kPa [VP 20/ 0·2, n= 8]) or rapid shallow (f=80 min^-1, V_T= 11 ±2 ml kg^-1 and PEEP = 0·2 or 0·4 kPa [VP 80/0·2, n= 6 and VP 80/0·4, n= 6]). The mean airway pressure was similar at VP 20/0·2 and VP 80/0·4. During administration of [⁹⁹Tc^m]DTPA aerosol all animals were ventilated under the same conditions (f=40 min^-1 and PEEP = 0·2 kPa). The pulmonary clearance rate expressed as the half-life time (T^1/2) of [⁹⁹Tc^m]DTPA was at VP 80/0·2 = 113 ± 31 min, at VP 80/0·4 = 70 ± 24 min (P < 0·01 compared to VP 80/0·2) and at VP 20/0·2 = 36± 18 min (P <0·001 compared to VP 80/0·2 and P <0·01 compared to VP 80/0·4). We conclude that the pulmonary clearance of [⁹⁹Tc^m]DTPA increases

• 1 during rapid shallow ventilation when PEEP is increased from 0·2 to 0·4 kPa;
• 2 during deep slow ventilation relative to rapid shallow ventilation even when the mean airway pressure is similar.

     

Effects of noninvasive positive pressure ventilatory support in non-COPD patients with acute respiratory insufficiency after early extubation

Objective: To investigate the effects of noninvasive positive pressure ventilation (NPPV) on pulmonary gas exchange, breathing pattern, intrapulmonary shunt fraction, oxygen consumption, and resting energy expenditure in patients with persistent acute respiratory failure but without chronic obstructive pulmonary disease (COPD) after early extubation. Design: Prospective study. Setting: Multidisciplinary intensive care unit of a university hospital. Patients: 15 patients after prolonged mechanical ventilation (> 72 h) with acute respiratory insufficiency after early extubation. Interventions: Criteria for early extubation were arterial oxygen tension (PaO₂) L 40 mm Hg (fractional inspired oxygen 0.21), arterial carbon dioxide tension (PaCO₂) K 55 mm Hg, pH > 7.32, respiratory rate K 40 breaths per min, tidal volume (V_T) L 3 ml/kg, rapid shallow breathing index K 190 and negative inspiratory force L 20 cmH₂O. After extubation, two modes of NPPV were applied [continuous positive airway pressure (CPAP) of 5 cmH₂O and pressure support ventilation (PSV) with 15 cmH₂O pressure support]. Measurements and main results: Oxygenation and ventilatory parameters improved during both modes of NPPV (p < 0.05): increase in PaO₂ of 11 mm Hg during CPAP and 21 mm Hg during PSV; decrease in intrapulmonary shunt fraction of 7 % during CPAP and 12 % during PSV; increase in tidal volume of 1 ml/kg during CPAP and 4 ml/kg during PSV; decrease in respiratory rate 6 breaths/min during CPAP and 9 breaths/min during PSV. Oxygen consumption (15 % during CPAP, 22 % during PSV) and resting energy expenditure (12 % during CPAP, 20 % during PSV) were reduced (p < 0.05). PaCO₂ decreased, whereas minute ventilation and pH increased during PSV (p < 0.05). The median duration of NPPV was 2 days. Two patients had to be reintubated. Conclusions: In non-COPD patients with persistent acute respiratory failure after early extubation, NPPV improved pulmonary gas exchange and breathing pattern, decreased intrapulmonary shunt fraction, and reduced the work of breathing. Received: 14 May 1999 Final revision received: 25 June 1999 Accepted: 6 July 1999     

Association of PEEP with two different inflation volumes in ARDS patients: effects on passive lung deflation and alveolar recruitment

Objective: To assess the effects of the association of positive end-expiratory pressure (PEEP) with different inflation volumes (V_T's) on passive lung deflation and alveolar recruitment in ARDS patients.¶Design: Clinical study using PEEP with two different V_T's and analyzing whether passive lung deflation and alveolar recruitment (Vrec) depend on end-inspired (EILV) or end-expired (EELV) lung volume in mechanically ventilated ARDS patients.¶Setting: Medical intensive care unit in a university hospital.¶Patients and participants: Six mechanically ventilated consecutive supine patients with ARDS.¶Interventions: Time-course of thoracic volume decay during passive expiration and Vrec were investigated in six ARDS patients ventilated on PEEP with baseline V_T (V_T,b) and 0.5V_T (0.5V_T,b), and on zero PEEP (ZEEP) with V_T,b. Time constants of the fast (τ ₁) and slow (τ ₂) emptying compartments, as well as resistances and elastances were also determined.¶Measurements and results: (a) the bi-exponential model best fitted the volume decay in all instances. The fast compartment was responsible for 84 ± 7 (0.5V_T,b) and 86 ± 5 % (V_T,b) on PEEP vs 81 ± 6 % (V_T,b) on ZEEP (P:ns) of the exhaled V_T, with τ ₁ of 0.50 ± 0.13 and 0.58 ± 0.17 s vs 0.35 ± 0.11 s, respectively; (b) only τ ₁ for V_T,b on PEEP differed significantly (P < 0.02) from the one on ZEEP, suggesting a slower initial emptying; (c) for the same PEEP, Vrec was higher with a higher volume (V_T,b) than at a lesser one (0.5V_T,b), reflecting the higher V_T.¶Conclusions: In mechanically ventilated ARDS patients: (a) the behavior of airway resistance seems to depend on the degree of the prevailing lung distension; (b) alveolar recruitment appears to be more important when higher tidal volumes are used during mechanical ventilation on PEEP; (c) PEEP changes the mechanical properties of the respiratory system fast-emptying compartment.     

THAM reduces CO2-associated increase in pulmonary vascular resistance – an experimental study in lung-injured piglets

IntroductionLow tidal volume (V_T) ventilation is recommended in patients with acute respiratory distress syndrome (ARDS). This may increase arterial carbon dioxide tension (PaCO₂), decrease pH, and augment pulmonary vascular resistance (PVR). We hypothesized that Tris(hydroxymethyl)aminomethane (THAM), a pure proton acceptor, would dampen these effects, preventing the increase in PVR.MethodsA one-hit injury ARDS model was established by repeated lung lavages in 18 piglets. After ventilation with V_T of 6 ml/kg to maintain normocapnia, V_T was reduced to 3 ml/kg to induce hypercapnia. Six animals received THAM for 1 h, six for 3 h, and six serving as controls received no THAM. In all, the experiment continued for 6 h. The THAM dosage was calculated to normalize pH and exhibit a lasting effect. Gas exchange, pulmonary, and systemic hemodynamics were tracked. Inflammatory markers were obtained at the end of the experiment.ResultsIn the controls, the decrease in V_T from 6 to 3 ml/kg increased PaCO₂ from 6.0±0.5 to 13.8±1.5 kPa and lowered pH from 7.40±0.01 to 7.12±0.06, whereas base excess (BE) remained stable at 2.7±2.3 mEq/L to 3.4±3.2 mEq/L. In the THAM groups, PaCO₂ decreased and pH increased above 7.4 during the infusions. After discontinuing the infusions, PaCO₂ increased above the corresponding level of the controls (15.2±1.7 kPa and 22.6±3.3 kPa for 1-h and 3-h THAM infusions, respectively). Despite a marked increase in BE (13.8±3.5 and 31.2±2.2 for 1-h and 3-h THAM infusions, respectively), pH became similar to the corresponding levels of the controls. PVR was lower in the THAM groups (at 6 h, 329±77 dyn∙s/m⁵ and 255±43 dyn∙s/m⁵ in the 1-h and 3-h groups, respectively, compared with 450±141 dyn∙s/m⁵ in the controls), as were pulmonary arterial pressures.ConclusionsThe pH in the THAM groups was similar to pH in the controls at 6 h, despite a marked increase in BE. This was due to an increase in PaCO₂ after stopping the THAM infusion, possibly by intracellular release of CO₂. Pulmonary arterial pressure and PVR were lower in the THAM-treated animals, indicating that THAM may be an option to reduce PVR in acute hypercapnia.     

Preliminary Report of a Mathematical Model of Ventilation and Intrathoracic Pressure Applied to Prehospital Patients with Severe Traumatic Brain Injury

Abstract

Background: Inadvertent hyperventilation is associated with poor outcomes from traumatic brain injury (TBI). Hypocapnic cerebral vasoconstriction is well described and causes an immediate and profound decrease in cerebral perfusion. The hemodynamic effects of positive-pressure ventilation (PPV) remain incompletely understood but may be equally important, particularly in the hypovolemic patient with TBI. Objective: Preliminary report on the application of a previously described mathematical model of perfusion and ventilation to prehospital data to predict intrathoracic pressure. Methods: Ventilation data from 108 TBI patients (76 ground transported, 32 helicopter transported) were used for this analysis. Ventilation rate (VR) and end-tidal carbon dioxide (PetCO₂) values were used to estimate tidal volume (V_T). The values for VR and estimated V_T were then applied to a previously described mathematical model of perfusion and ventilation. This model allows input of various lung parameters to define a pressure–volume relationship, then derives mean intrathoracic pressure (MITP) for various V_T and VR values. For this analysis, normal lung parameters were utilized. Separate analyses were performed assuming either fixed or variable PaCO₂–PetCO₂ differences. Ground and air medical patients were compared with regard to VR, PetCO₂, estimated V_T, and predicted MITP. Results: A total of 10,647 measurements were included from the 108 TBI patients, representing about 13 minutes of ventilation per patient. Mean VR values were higher for ground patients versus air patients (21.6 vs. 19.7 breaths/min; p < 0.01). Estimated V_T values were similar for ground and air patients (399 mL vs. 392 mL; p = NS) in the fixed model but not the variable (636 vs. 688 mL, respectively; p < 0.01). Mean PetCO₂ values were lower for ground versus air patients (30.6 vs. 33.8 mmHg; p < 0.01). Predicted MITP values were higher for ground versus air patients, assuming either fixed (9.0 vs. 8.1 mmHg; p < 0.01) or variable (10.9 vs. 9.7 mmHg; p < 0.01) PaCO₂–PetCO₂ differences. Conclusions: Predicted MITP values increased with ventilation rates. Future studies to externally validate this model are warranted.     

End-tidal carbon dioxide as a measure of arterial carbon dioxide during intermittent mandatory ventilation

To determine if end-tidal carbon dioxide tension (PetCO₂) is a clinically reliable indicator of arterial carbon dioxide tension (PaCO₂) under conditions of heterogeneous tidal volumes and ventilation-perfusion inequality, we examined the expiratory gases of 25 postcardiotomy patients being weaned from ventilator support with intermittent mandatory ventilation. Using a computerized system that automatically sampled airway flow, pressure, and expired carbon dioxide tension, we were able to distinguish spontaneous ventilatory efforts from mechanical ventilatory efforts. ThePetCO₂ values varied widely from breath to breath, and the arterial to end-tidal carbon dioxide tension gradient was appreciably altered during the course of several hours. About two-thirds of the time, thePetCO₂ of spontaneous breaths was greater than that of ventilator breaths during the same 70-second sample period. The most accurate indicator of PaCO₂ was the maximalPetCO₂ value in each sample period, the correlation coefficient being 0.768 (P < 0.001) and the arterial to end-tidal gradient being 4.24 ± 4.42 mm Hg (P < 0.01 compared with all other measures). When all values from an 8-minute period were averaged, stability was significantly improved without sacrificing accuracy. We conclude that monitoring the maximalPetCO₂, independent of breathing pattern, provides a clinically useful indicator of PaCO₂ in postcardiotomy patients receiving intermittent mandatory ventilation.     

Positive end expiratory pressure and critical oxygenation during transport in ventilated patients

Transportation of patients critically dependent on positive end expiratory pressure (PEEP) can be problematic, as a patient of ours with adult respiratory distress syndrome (ARDS) and bilateral broncho-pleural fistulae demonstrated. He required intermittent positive pressure ventilation (IPPV) (Siemens 900C) with 100% O₂ and PEEP of 2 kPa to maintain his arterial O₂ saturation (SaO₂)>90%. Severe hypoxemia (SaO₂<75%) occurred on change to a portable ventilator (Oxylog, Dräger) with a PEEP valve (Ambu 20) at its expiratory port, despite adjusting the valve to 2 kPa, continuing use of 100% O₂, and varying the ventilatory pattern. The problem appeared due to loss of PEEP because of gas leak from the lungs via his intercostal catheters. It was solved by introducing a continuous O₂ flow of 51/min into the circuit between the Oxylog non-rebreathing valve and endotracheal tube. We used a model lung to investigate the effect of a gas leak from the lungs or circuit on the performance of the Oxylog IPPV/PEEP system. Lung compliance and ventilatory pattern were adjusted so that tidal volume (V_T)=0.61, peak inspiratory Airway pressure (PIP)=5 kPa, PEEP=1.5 kPa, and respiratory rate=10/min. A small leak was introduced from the lung resulting in a decrease in PIP, V_T, and PEEP. Adjustment of ventilator minute volume to restore PIP to 5 kPa failed to restore PEEP, airway pressure continuing to fall throughout the expiratory pause. PEEP was restored by providing a compensatory flow of O₂ of 5l/min to the system between the Oxylog nonrebreathing valve and the lung. We conclude that significant loss of PEEP can occur in patients with gas leaks from the lung when ventilators, such as the Oxylog, are used that do not provide a compensatory flow of gas into the lung during expiration and the expiratory pause. If the patient is critically dependent on PEEP this loss will result in severe hypoxemia.     

Calculation algorithms alter the breath‐by‐breath gas exchange values when abrupt changes in ventilation occur

The automatic metabolic units calculate breath‐by‐breath gas exchange from the expiratory data only, applying an algorithm (‘expiration‐only’ algorithm) that neglects the changes in the lung gas stores. These last are theoretically taken into account by a recently proposed algorithm, based on an alternative view of the respiratory cycle (‘alternative respiratory cycle’ algorithm). The performance of the two algorithms was investigated where changes in the lung gas stores were induced by abrupt increases in ventilation above the physiological demand. Oxygen, carbon dioxide fractions and ventilatory flow were recorded at the mouth in 15 healthy subjects during quiet breathing and during 20‐s hyperventilation manoeuvres performed at 5‐min intervals in resting conditions. Oxygen uptakes and carbon dioxide exhalations were calculated throughout the acquisition periods by the two algorithms. Average ventilation amounted to 6·1 ± 1·4 l min^?1 during quiet breathing and increased to 41·8 ± 27·2 l min^?1 during the manoeuvres (P<0·01). During quiet breathing, the two algorithms provided overlapping gas exchange data and noise. Conversely, during hyperventilation, the ‘alternative respiratory cycle’ algorithm provided significantly lower gas exchange data as compared to the values yielded by the ‘expiration‐only’ algorithm. For the first breath of hyperventilation, the average values provided by the two algorithms amounted to 0·37 ± 0·34 l min^?1 versus 0·96 ± 0·73 l min^?1 for O₂ uptake and 0·45 ± 0·36 l min^?1 versus 0·80 ± 0·58 l min^?1 for exhaled CO₂ (P<0·001 for both). When abrupt increases in ventilation occurred, such as those arising from a deep breath, the ‘alternative respiratory cycle’ algorithm was able to halve the artefactual gas exchange values as compared to the ‘expiration‐only’ approach.     

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.