Changes in airway dead space in response to methacholine provocation in normal subjects

Measurements of bronchial hyper-responsiveness rely on sensitive techniques for measurement of bronchoconstriction, ideally based on tidal breathing. A potentially useful technique is measurement of airway dead space (V_Daw), which reflects the volume of the conducting airways. The aim of this study was to evaluate measurements of V_Daw with the single breath test for CO₂ (SBT-CO₂), compared to spirometric measurements, as a method of measuring bronchial response to methacholine challenge. Nineteen healthy adults were studied. Dosimetric methacholine challenge tests were performed on two study days. Forced expirations or the SBT-CO₂ were used to assess the response. There were dose-dependent reductions in the spirometric measurements, with a 10 ± 10% reduction from the baseline value of forced expiratory volume at the highest dose of methacholine. There was a dose-dependent reduction from the baseline value of V_Daw by 19 ± 9% at the highest dose. There was also a dose-dependent increase in the slope of the alveolar plateau of the SBT-CO₂. This study provides support for measurement of V_Daw as a means of evaluating bronchial responsiveness after methacholine challenge. In a group of healthy adults, this method shows a greater response but with similar dispersion as measurement of forced expiratory volume after methacholine challenge.     

Aspiration of dead space allows normocapnic ventilation at low tidal volumes in man

Objective: Aspiration of dead space (ASPIDS) improves carbon dioxide (CO₂) elimination by replacing dead space air rich in CO₂ with fresh gas during expiration. The hypothesis was that ASPIDS allows normocapnia to be maintained at low tidal volumes (V_T). Design: Prospective study. Setting: Adult intensive care unit in a university hospital. Patients: Seven patients ventilated for neurological reasons were studied. All patients were clinically and haemodynamically stable and monitored according to clinical needs. Interventions: ASPIDS implies that, during expiration, gas is aspirated through a catheter inserted in the tracheal tube. Simultaneously, a compensatory flow of fresh gas is injected into the inspiratory line. ASPIDS was achieved with a computer/ventilator system controlling two solenoid valves for aspiration and injection. Results: At the basal respiratory rate of 12.6 breaths min^–1, with ASPIDS V_T decreased from 602 to 456 ml, as did the airway pressures to a corresponding degree. PaCO₂ and PaO₂ remained stable. At a frequency of 20 breaths min^–1, with ASPIDS V_T was further reduced to 305 ml with preserved normocapnia. ASPIDS did not interfere with the positive end-expiratory pressure (PEEP) level. No intrinsic PEEP developed. All patients remained stable. No haemodynamic or other side effects of ASPIDS were noticed. Conclusion: The results of this study suggest that ASPIDS may be a useful and safe modality of mechanical ventilation that limits alveolar pressure and minute ventilation requirements while keeping PaCO₂ constant. Received: 21 December 1998 Final revision received: 28 April 1999 Accepted: 3 May 1999     

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.     

Comparison of different methods for dead space measurements in ventilated newborns using CO2-volume plot

Objective: The aim of the study was to test the applicability of Ventrak 1550/Capnogard 1265 (V-C) for respiratory dead space (Vd) measurement and to determine anatomic (V_Dana), physiologic (V_Dphys), and alveolar dead spaces (V_Dalv) in ventilated neonates. Design: Prospective study. Setting: Neonatal intensive care unit. Patients: 33 investigations in 22 ventilated neonates; median gestational age 34.5 weeks (range 27–41), median birthweight 2658 g (range 790–3940). Method: The single-breath CO₂ test (SBT-CO₂) and transcutaneous partial pressure of carbon dioxide (PCO₂) were recorded simultaneously and Vd was determined (1) automatically (V-C software), (2) by interactive analysis of the PCO₂ volume plot, and (3) manually by Bohr/Enghoff equations using data obtained by V-C. Results: Vd measurements were possible in all cases by method 3 but not possible by methods 1 and 2 in 22 of 33 investigations (67 %), especially in preterm neonates, because of disturbed signals. V_Dana/kg (1.6 ± 0.6 ml/kg, mean ± SD), V_Dana/tidal volume (Vt) (0.36 ± 0.09) were lower compared to published data in spontaneously breathing infants, whereas V_Dphys/kg (2.3 ± 0.9 ml/kg) and V_Dphys/Vt (0.50 ± 0.12) are comparable to data obtained from the literature. Five minutes after insertion of the sensor (dead space 2.6 ml) into the ventilatory circuit, the transcutaneous PCO₂ rose above baseline for 3.2 % (patients > 2500 g) and 5.7 % (patients < 2500 g). The time necessary for one analysis was 50–60 min. Conclusion: In ventilated newborns, dead space measurements were possible only in one-third by SBT-CO₂, but in all cases by Bohr/Enghoff equations. Improved software could further reduce the time needed for one analysis. Received: 8 December 1998 Accepted: 19 April 1999     

Measurement of pulmonary CO2 elimination must exclude inspired CO2 measured at the capnometer sampling site

Objective. The pulmonary elimination of the volume of CO₂ per breath (VCO₂/br, integration of product of airway flow ( ) and PCO₂ over a single breath) is a sensitive monitor of cardio-pulmonary function and tissue metabolism. Negligible inspired PCO₂ results when the capnometry sampling site (SS) is positioned at the entry of the inspiratory limb to the airway circuit. In this study, we test the hypothesis that moving SS lungward will result in significant inspired CO₂ (VCO₂[I]), that needs to be excluded from VCO₂/br.Methods. We ventilated a mechanical lung simulator with tidal volume (V_T) of 800 mL at 10 breaths/min. CO₂ production, generated by burning butane in a separate chamber, was delivered to the lung. Airway and PCO₂ were measured (Capnomac Ultima, Datex), digitized (100 Hz for 60 s), and stored by microcomputer. Then, computer algorithms corrected for phase diferences between and PCO₂ and calculated expired and inspired VCO₂ (VCO₂[E] and VCO₂[I]) for each breath, whose difference equalled overall VCO₂/br. The lung and Y-adapter (where the inspiratory and expiratory limbs of the circuit joined) were connected by the SS and a connecting tube in varying order.Results. During ventilation of the lung model (V_T = 800 ml) with SS adjacent to the inspiratory limb, VCO₂[E] was 16.8± 0.4 ml and VCO₂[I] was 1.1 ±0.1 ml, resulting in overall VCO₂/br (VCO₂[E] —VCO₂[I]) of 15.7 ± 0.4 ml. If VCO₂[I] was ignored in the determination of VCO₂/br, then the %error that VCO₂[E] overestimated VCO₂/br was 7.2± 0.3%. This %error significantly increased (p < 0.05, Student's t-test) when V_T was decreased to 500 mL (%error = 12.4 ± 0.8%) or when SS was moved to the lungward side of a 60 mL connecting tube (VCO₂[I] = 2.8 ± 0.2, %error = 18.2 ± 1.6) or a 140 mL tube (VCO₂[I] = 5.9±03 mL, %error = 37.5±3.3).Conclusions. When the SS was moved lungward from the inspiratory limb, instrumental dead space (VD _INSTR) increased and, at end-expiration, contained exhaled CO₂ from the previous breath. During the next inspiration, this CO₂ was rebreathed relative to SS (i.e. VCO₂[I]), and contributed to VCO₂[E]. Thus, VCO₂[E] overestimated VCO₂/br (%error) by the amount of rebreathing, which was exacerbated by largerVD _INSTR (increased VCO₂[I]) or smaller V_T (increased VCO₂[I]-to-VCO₂/br ratio).     

Comparison between ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia in healthy sleeping man

Summary. Ventilatory and mouth occlusion pressure (P_0·1) responses to progressive isocapnic-hypoxia and hyperoxic-hypercapnia were compared in eleven healthy sleeping men during the same night. Hypoxic and hypercapnic responses were determined during wakefulness, non-rapid and rapid-eye-movement sleep. The following parameters were measured: minute ventilation (V?E), tidal volume (V_T), ‘duty cycle’ (T_l/T_T), mean inspiratory flow rate (V_T/T_l) and P_0·1, an index of the neuromuscular inspiratory drive. To allow a direct comparison between the two types of chemostimuli, responses were characterized by the value of the different parameters at ‘equivalent’ levels of hypoxia and hypercapnia, i.e., at levels which produced the same P_0·1 during wakefulness: an oxyhaemoglobin saturation (Sao₂) of 94% during the isocapnic-hypoxic tests (P_ETco₂=42·5±1·2 mmHg) was found to be equivalent to a P_etco₂ of 47·4±3·7 mmHg during hypoxic-hypercapnic tests. For both tests, the arousal levels of the stimulus and of P_0·1 were similar in all sleep stages. Sleep did not significantly modify P_0·1 or breathing pattern responses to hypoxia (Sao₂=94%). In contrast, at the ‘equivalent’ level of hypercapnic stimulation, P_0·1 (P<0·05) and V?_E (P<0·01) responses were significantly impaired, particularly in REM sleep, with a decrease in V_T (P<0·01) and V_T/T_l (P<0·05) responses. The results suggest that CO₂ intracranial receptor mechanisms are more affected by sleep than the O₂ peripheral receptor activity.     

Comparison of volumetric capnography and mixed expired gas methods to calculate physiological dead space in mechanically ventilated ICU patients

Introduction

Physiological dead space should be a routine measurement in ventilated patients but measuring dead space using the Douglas bag (DB) method is cumbersome and requires corrections for compressed ventilator gas. These factors make this method impractical in the critical care setting. Volumetric capnography (VCAP) offers a relatively simple solution to calculating dead space. Few studies have been conducted to directly compare dead space measured by VCAP and the DB method in critically unwell adults.

Method

Prospective observational study of 48 mechanically ventilated adults ICU patients. Dead space was calculated simultaneously using VCAP (CO₂SMO) and the Bohr–Enghoff equation. In total, 168 paired readings were taken. Single-breath CO₂ waveform areas under the curve were computed automatically by software to calculate physiological dead space. The calculated value of $ P_{{\bar{E}_{{{\text{CO}}_{2} }} }} $ was also recorded from the CO₂SMO device. Exhaust ventilator gas was collected in a 10-l mixing chamber. $ P_{{\bar{E}_{{{\text{CO}}_{2} }} }} $ was measured in the chamber following correction for compressed gas.

Results

The study demonstrated good agreement between physiological V _D/V _T calculated by VCAP and corrected (mean bias 0.03), and uncorrected (mean bias 0.02) Bohr–Enghoff method. There was good correlation between the two methods of measurement (VCAP vs corrected r ²?=?0.90 P?<?0.001, VCAP vs uncorrected r ²?=?0.90, P?<?0.001). There was good correlation between $ P_{{\bar{E}_{{{\text{CO}}_{2} }} }} $ calculated by the CO₂SMO and in the exhaust collected gas (mean bias 0.08).

Conclusions

VCAP shows good agreement with Douglas Bag method in measuring physiological V _D/V _T over a wide range of dead space fractions.     

Nitrogen dead space in heavy smokers aged 44–58 years

Summary. Functional and alveolar dead spaces for nitrogen (V_df and V_dalv) were calculated in a population of 20 male and 20 female heavy smokers and compared to data from static and forced spirometry (functional residual capacity [FRC], residual volume [RV], lung clearance index [LCI] and volume of trapped gas [VTG]) obtained with the same multiple-breath nitrogen wash-out as the dead spaces, and to variables considered sensitive to small airways disease measured with a single-breath nitrogen elimination (closing volume in per cent of vital capacity [CV%], closing capacity in per cent of total lung capacity [CC%] and slope index [SI]). Both nitrogen dead spaces increased with tidal volume in smokers as well as in healthy non-smokers. The majority of smokers were outside the predicted mean+2 SD for VTG (75%), CC and V_Dalv (70%) and SI (65%). The following variables were less sensitive for disclosing abnormality: CV (55%), RV (53%), LCI (38%) and forced expired volume in the first second (FEV₁, 33%). If high sensitivity is considered preferable in epidemiological studies, the nitrogen dead spaces are equally as sensitive as the better of earlier described tests, and significantly superior to LCI and FEV₁. Being tests that measure alveolar distribution of inhaled gas, they are probably sensitive to small airways disease.     

PaCO2 and alveolar dead space are more relevant than PaO2/FiO2 ratio in monitoring the respiratory response to prone position in ARDS patients: a physiological study

Introduction  

Our aims in this study were to report changes in the ratio of alveolar dead space to tidal volume (VD_alv/V_T) in the prone position (PP) and to test whether changes in partial pressure of arterial CO₂ (PaCO₂) may be more relevant than changes in the ratio of partial pressure of arterial O₂ to fraction of inspired O₂ (PaO₂/FiO₂) in defining the respiratory response to PP. We also aimed to validate a recently proposed method of estimation of the physiological dead space (VD_physiol/V_T) without measurement of expired CO₂.     

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.     

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25–40) in the LHD group and 44 W (33–49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31·0 ± 5·5 to 8·8 ± 5·0 mmHg in the LHD group, compared with from 13·7 ± 1·0 to 2·1 ± 2·4 mmHg in the controls, while ventilation/O₂ intake ratio (V˙/V˙O₂) and physiological dead space/tidal volume ratio (V_D/V_T) showed a tendency to rise, from 36·3 ± 8·8 to 39·2 ± 7·4, and from 0·35 ± 0·11 to 0·39 ± 0·09, respectively, in the LHD group, and from 27·5 ± 3·1 to 28·7 ± 5·3, and from 0·19 ± 0·09 to 0·21 ± 0·12 in the controls. Mixed venous O₂ tension (PvO ₂) showed a marked decline from 3·60 ± 0·33 to 3·26 ± 0·36 kPa in the LHD group, as compared with from 3·94 ± 0·28 to 3·71 ± 0·29 kPa in the controls, while the calculated physiologic shunt (Q˙_s/Q˙_t) suggested improved alveolo‐arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia‐induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.     

Respiratory effects of tracheal gas insufflation in spontaneously breathing COPD patients

Objective To evaluate the effect of tracheal gas insufflation (TGI) in spontaneously breathing, intubated patients with chronic obstructive pulmonary disease (COPD) undergoing weaning from the mechanical ventilation.Design A prospective study in humans.Setting Polyvalent intensive care unit (14-bed ICU) in a 700-bed general university hospital.Patients Twelve patients with chronic obstructive pulmonary disease (COPD) who required intubation and mechanical ventilation were studied. All patients met standard criteria for weaning from mechanical ventilation. Seven patients (group 1) had been transorally intubated during episodes of acute respiratory failure. Five patients, all men (group 2), had previously undergone tracheostomy and had a transtracheal tube in place.Interventions Intratracheal, humidified, O₂-mixture insufflation (TGI) was given via a catheter placed in distal or proximal position. Gas delivered through the intratracheal catheter was blended to match the fractional of inspired gas through the endotracheal tube. Continuous flows of 3 and 6 l/min in randomized order were used in each catheter position. Prior to data collection at each stage, an equilibration period of at least 30 min was observed, and thereafter blood gases were analyzed every 5 min. A new steady state was assumed to have been established when values of bothP _aCO₂ and CO₂ changed by less than 5% between adjacent measurements. The last values of blood gases were taken as representative. The new steady state was confirmed within 35–50 min. Baseline measurements with zero were made at the beginning and end of the experiment.Results This study shows that V_T, MV,P _aCO₂, and V_D/V_T are reduced in a flow-dependent manner when gas is delivered through an oral-tracheal tube (group 1). The distal catheter position was more effective than the proximal one. In contrast, when gas was delivered through tracheostomy (group 2), TGI was ineffective in the proximal position and less effective than in group 1 in distal position.Conclusion Under the experimental conditions, tracheal gas insufflation decreased dead space, increased alveolar ventilation and possibly reduced work of breathing. From the preliminary data reported here, we believe that TGI may help patients experiencing difficulty during weaning.     

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     

High flow nasal cannula: Influence of gas type and flow rate on airway pressure and CO2 clearance in adult nasal airway replicas

BackgroundHigh flow nasal cannula therapy is a form of respiratory support which delivers high flow rates of heated, humidified gas to the nares via specialized cannula. Two primary mechanisms of action attributed to the therapy are the provision of positive airway pressure as well as clearance of CO₂-rich exhaled gas from the upper airways.MethodsPhysiologically accurate nose-throat airway replicas were connected at the trachea to a lung simulator, where CO₂ was supplied to mimic the CO₂ content in exhaled gas. Cannula delivered either air, oxygen or heliox (80/20%volume helium/oxygen) to the replicas at flow rates ranging from 0 to 60 l/min. Five replicas and three cannulas were compared. Tracheal pressure and CO₂ concentration were continuously measured. The lung simulator provided breaths with tidal volume of 500 ml and frequency of 18 breaths/min. Additional clearance measurements were conducted for tidal volume and breathing frequency of 750 ml and 27 breaths/min, respectively.FindingsCannula flow rate was the dominant factor governing CO₂ concentration. Average CO₂ concentration decreased with increasing cannula flow rate, but above 30 L/min this effect was less pronounced. Tracheal positive end-expiratory pressure increased with flow rate and was lower for heliox than for air or oxygen. A predictive correlation was developed and used to predict positive end-expiratory pressure for a given cannula size as a function of supplied flow rate and occlusion of the nares.InterpretationCompared with administration of air or oxygen, administration of heliox is expected to result in similar CO₂ clearance from the upper airway, but markedly lower airway pressure.     

Physiological effects of reduced tidal volume at constant minute ventilation and inspiratory flow rate in acute respiratory distress syndrome

Objective To assess the effect of changes in tidal volume (V _T) with a constant inspiratory flow and minute ventilation on gas exchange and oxygen transport in acute respiratory distress syndrome (ARDS).Design A crossover study of threeV _T in two study groups, using patients as their own controls.Setting: A medical-surgical intensive care unit in a tertiary care center.Patients Eight patients with ARDS and seven postoperative cardiac surgery patients with uncomplicated recoveries were studied during volume-controlled mechanical ventilation.Interventions During controlled mechanical ventilation, patients were first ventilated with aV _T of 9–11 ml/kg.V _T was then increased to 12–14 ml/kg (+25%) for 30 min and subsequently decreased to 6–8 ml/kg (–25%) for 30 min by adjusting the respiratory rate (RR) while the inspiratory flow rate, , and inspiratory duty cycle (T_L/T_TOT) were kept constant. At the end, patients were ventilated with the baseline settings for another 30 min.Measurements and results V _E, carbon dioxide production and oxygen consumption were measured continuously with a gas exchange monitor, and cardiac output and arterial and mixed venous blood samples were taken at the end of each 30-min period to assess CO₂ removal and oxygen transport. Alveolar minute ventilation and the deadspace to tidal volume ratio (V _D/V _T) were calculated from the Bohr equation. Despite large changes inV _T, arterial oxygenation (P _aO₂) and oxygen transport were unchanged throughout the study. WhenV _T was increased, physiologicalV _D increased from 448±34 ml to 559±46 ml (mean±SE) in ARDS (P<0.001) and from 281±22 ml to 357±35 ml in CABG (P<0.05). With the smallV _T,V _D decreased to 357±22 ml in ARDS (P<0.01), and to 234±24 ml in CABG (P<0.05). In ARDS,V _D/V _T decreased from 0.57±0.03 to 0.55±0.03 (P<0.05) with the largeV _T, and increased to 0.60±0.03 (P<0.01), whenV _T was reduced. In CABG,V _D/V _T did not change significantly. ARDS patients had a higherP _aCO₂ than cardiac patients (P<0.001), and only minor changes inP _aCO₂ were observed (for ARDS and CABG respectively, baseline 5.9±0.3 kPa and 4.1±0.1 kPa, largeV _T 5.7±0.3 kPa and 4.1±0.2 kPa, smallV _T 6.2±0.3 kPa and 4.2±0.2 kPa;P<0.05).Conclusions Tidal volumes can be reduced to 6–8 ml/kg in ARDS patients without compromising oxygen transport, while adequate CO₂ elimination can be maintained.     

How do changes in exhaled CO<Subscript>2</Subscript> measure changes in cardiac output? A numerical analysis model

Objective  

In a previous study in anesthetized animals, the slope of percent decreases in exhaled CO₂ versus percent decreases in cardiac output ( [(Q)\dot]\scT, \dot{\rm Q}{\sc{T,}} inflation of vena cava balloons) was 0.73. To examine the mechanisms underlying this exhaled CO₂- [Q\dot]\sc T {\dot{\hbox{Q}}{\sc T}} relationship, an iterative numerical analysis computer model of non-steady state CO₂ kinetics was developed.     

Reproducibility of the respiratory dead space measurements in mechanically ventilated children using the CO<Subscript>2</Subscript>SMO monitor

Objectives To assess the reproducibility of respiratory dead space measurements in ventilated children.Design Prospective study.Setting University pediatric intensive care unit.Patients Thirty-two mechanically ventilated children (0.13–15.4 years) who were clinically stable.Methods The single-breath CO₂ test (SBT-CO₂) was recorded using the CO₂SMO Plus from the mean of 30 ventilatory cycles during 1 h (at T0, T15, T30, T45, and T60). Airway dead space was determined automatically (Novametrix Medical Systems, USA), and manually by Bohr- Enghoff equations using data obtained by SBT-CO₂. At the end of the study period, arterial blood gas was sampled in order to calculate alveolar and physiologic dead space. Intrasubject reproducibility of measurements was evaluated by the intraclass correlation coefficient. Two-way analysis of variance was used to evaluate the relationships between time and measurements. The two methods for calculating airway dead space were compared by using two-tailed Students t-test and Bland-Altman analysis.Results Airway dead space measurement had a good reproducibility during the 1-h period, whatever the method used (intraclass correlation coefficient: 0.84 to 0.87). No significant difference was observed with time. Airway dead space values from the SBT-CO₂ method were smaller than those from Bohr-Enghoff equations. Physiologic dead space values from the SBT-CO2 method were similar to those from Bohr-Enghoff equations.Conclusion The measurement of airway dead space by the CO₂SMO Plus was reproducible over a 1-h period in children requiring mechanical ventilation, provided ventilatory parameters were constant throughout the study. SBT-CO₂ analysis may provide a bedside non-invasive monitoring of volumetric capnography.     

Atherosclerotic plaques in the internal carotid artery and associations with lung function assessed by different methods

Background: Previous studies on associations between reduced lung function and cardiovascular disease (CVD) have mainly been based on forced expiratory volume in 1‐s (FEV₁) and vital capacity (VC). This study examined potential associations between five different lung function variables and plaques in the internal carotid artery (ICA). Methods: Subjects (n = 450) from a previous population‐based respiratory questionnaire survey [current smokers without lower respiratory symptoms, subjects with a self‐reported diagnosis of chronic obstructive pulmonary disease (COPD) and never‐smokers without lower respiratory symptoms] were examined using spirometry, body plethysmography and measurements of diffusing capacity for CO (D_L,CO). Plaques in the ICA were assessed by ultrasonography. Results: Two hundred and twenty subjects were current smokers, 139 ex‐smokers and 89 never‐smokers. COPD was diagnosed in 130 subjects (GOLD criteria). Plaques in the ICA were present in 231 subjects (52%). General linear analysis with adjustment for established risk factors for atherosclerosis, including C‐reactive protein, showed that D_L,CO was lower [77·4% versus 83·7% of predicted normal (PN), P = 0·014] and residual volume (RV) was higher (110·3% versus 104·8% of PN, P = 0·020) in subjects with than without plaques in the ICA. This analysis did not show any statistically significant association between plaques and FEV₁ or VC. Conclusion: The occurrence of plaques in the ICA was associated with low D_L,CO and high RV, but not significantly with FEV₁ or COPD status. The results suggest that the relationships between reduced lung function, COPD and CVD are complex and not only linked to bronchial obstruction and low‐grade systemic inflammation.     

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.