Measurement Of Dead Space Research Articles

Differences in Exercise Capacity, Ventilatory Efficiency, and Gas Exchange between Patients with Pulmonary Arterial Hypertension and Chronic Thromboembolic Pulmonary Hypertension Residing at High Altitude.

Cardiopulmonary exercise testing (CPET) assesses exercise capacity and causes of exercise limitation in patients with pulmonary hypertension (PH). At altitude, changes occur in the ventilatory pattern and a decrease in arterial oxygen pressure in healthy; these changes are increased in patients with cardiopulmonary disease. Our objective was to compare the response to exercise and gas exchange between patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) residing at the altitude of Bogotá (2640 m). All patients performed an incremental CPET with measurement of oxygen consumption ( ), dead space (VD/VT), ventilatory equivalents (VE/ ), and alveolar-arterial oxygen gradient ( ). test and one-way analysis of variance were used for comparisons between PAH and CTEPH. We included 53 patients, 29 with PAH, 24 with CTEPH, and 102 controls as a reference of the normal response to exercise at altitude. CTEPH patients had a higher New York Health Association (NYHA) functional class than PAH (p = 0.037). There were no differences between patients with PAH and CTEPH in hemodynamics and % of predicted (67.8 18.7 vs. 66.0 19.8, p 0.05), but those with CTEPH had higher dyspnea, VD/VT (0.36 0.09 vs. 0.23 0.9, p 0.001), VE/ (45.8 7.1 vs. 39.3 5.6, p 0.001), and (19.9 7.6 vs. 13.5 7.6, p 0.001) than PAH patients. At altitude, patients with PH present severe alterations in gas exchange during exercise. There were no differences in exercise capacity between PAH and CTEPH, but patients with CTEPH had more dyspnea and greater alterations in gas exchange during exercise. CPET made it possible to identify alterations related to the pathophysiology of CTEPH that could explain the functional class and dyspnea in these patients.

COVID-19 ARDS Is Characterized by Increased Dead Space Ventilation Compared With Non-COVID ARDS.

ARDS in patients with coronavirus disease 2019 (COVID-19) is characterized by microcirculatory alterations in the pulmonary vascular bed, which could increase dead-space ventilation more than in non-COVID-19 ARDS. We aimed to establish if dead-space ventilation is different in patients with COVID-19 ARDS when compared with patients with non-COVID-19 ARDS. A total of 187 subjects with COVID-19 ARDS and 178 subjects with non-COVID-19 ARDS who were undergoing invasive mechanical ventilation were included in the study. The association between the ARDS types and dead-space ventilation, compliance of the respiratory system, subjects' characteristics, organ failures, and mechanical ventilation was evaluated by using data collected in the first 24 h of mechanical ventilation. Corrected minute ventilation (V˙E), a dead-space ventilation surrogate, was higher in the subjects with COVID-19 ARDS versus in those with non-COVID-19 ARDS (median [interquartile range] 12.6 [10.2-15.8] L/min vs 9.4 [7.5-11.6] L/min; P < .001). Increased corrected V˙E was independently associated with COVID-19 ARDS (odds ratio 1.24, 95% CI 1.07-1.47; P = .007). The best compliance of the respiratory system, obtained after testing different PEEPs, was similar between the subjects with COVID-19 ARDS and the subjects with non-COVID-19 ARDS (mean ± SD 38 ± 11 mL/cm H2O vs 37 ± 11 mL/cm H2O, respectively; P = .61). The subjects with COVID-19 ARDS received higher median (interquartile range) PEEP (12 [10-14] cm H2O vs 8 [5-9] cm H2O; P < .001) and lower median (interquartile range) tidal volume (5.8 [5.5-6.3] mL/kg vs 6.6 [6.1-7.3] mL/kg; P < .001) than the subjects with non-COVID-19 ARDS, being these differences maintained at multivariable analysis. In the multivariable analysis, the subjects with COVID-19 ARDS showed a lower risk of anamnestic arterial hypertension (odds ratio 0.18, 95% CI 0.07-0.45; P < .001) and lower neurologic sequential organ failure assessment score (odds ratio 0.16, 95% CI 0.09-0.27; P < .001) than the subjects with non-COVID-19 ARDS. Indirect measurements of dead space were higher in subjects with COVID-19 ARDS compared with subjects with non-COVID-19 ARDS. The best compliance of the respiratory system was similar in both ARDS forms provided that different PEEPs were applied. A wide range of compliance is present in every ARDS type; therefore, the setting of mechanical ventilation should be individualized patient by patient and not based on the etiology of ARDS.

End-tidal to arterial PCO2 ratio: a bedside meter of the overall gas exchanger performance

BackgroundThe physiological dead space is a strong indicator of severity and outcome of acute respiratory distress syndrome (ARDS). The “ideal” alveolar PCO2, in equilibrium with pulmonary capillary PCO2, is a central concept in the physiological dead space measurement. As it cannot be measured, it is surrogated by arterial PCO2 which, unfortunately, may be far higher than ideal alveolar PCO2, when the right-to-left venous admixture is present. The “ideal” alveolar PCO2 equals the end-tidal PCO2 (PETCO2) only in absence of alveolar dead space. Therefore, in the perfect gas exchanger (alveolar dead space = 0, venous admixture = 0), the PETCO2/PaCO2 is 1, as PETCO2, PACO2 and PaCO2 are equal. Our aim is to investigate if and at which extent the PETCO2/PaCO2, a comprehensive meter of the “gas exchanger” performance, is related to the anatomo physiological characteristics in ARDS.ResultsWe retrospectively studied 200 patients with ARDS. The source was a database in which we collected since 2003 all the patients enrolled in different CT scan studies. The PETCO2/PaCO2, measured at 5 cmH2O airway pressure, significantly decreased from mild to mild–moderate moderate–severe and severe ARDS. The overall populations was divided into four groups (~ 50 patients each) according to the quartiles of the PETCO2/PaCO2 (lowest ratio, the worst = group 1, highest ratio, the best = group 4). The progressive increase PETCO2/PaCO2 from quartile 1 to 4 (i.e., the progressive approach to the “perfect” gas exchanger value of 1.0) was associated with a significant decrease of non-aerated tissue, inohomogeneity index and increase of well-aerated tissue. The respiratory system elastance significantly improved from quartile 1 to 4, as well as the PaO2/FiO2 and PaCO2. The improvement of PETCO2/PaCO2 was also associated with a significant decrease of physiological dead space and venous admixture. When PEEP was increased from 5 to 15 cmH2O, the greatest improvement of non-aerated tissue, PaO2 and venous admixture were observed in quartile 1 of PETCO2/PaCO2 and the worst deterioration of dead space in quartile 4.ConclusionThe ratio PETCO2/PaCO2 is highly correlated with CT scan, physiological and clinical variables. It appears as an excellent measure of the overall “gas exchanger” status.

Near-real-time pulmonary shunt and dead space measurement with micropore membrane inlet mass spectrometry in pigs with induced pulmonary embolism or acute lung failure

The multiple inert gas elimination technique (MIGET) using gas chromatography (GC) is an established but time-consuming method of determining ventilation/perfusion (VA/Q) distributions. MIGET-when performed using Micropore Membrane Inlet Mass Spectrometry (MMIMS)-has been proven to correlate well with GC-MIGET and reduces analysis time substantially. We aimed at comparing shunt fractions and dead space derived from MMIMS-MIGET with Riley shunt and Bohr dead space, respectively. Thirty anesthetized pigs were randomly assigned to lavage or pulmonary embolism groups. Inert gas infusion (saline mixture of SF6, krypton, desflurane, enflurane, diethyl ether, acetone) was maintained, and after induction of lung damage, blood and breath samples were taken at 15-min intervals over 4h. The samples were injected into the MMIMS, and resultant retention and excretion data were translated to VA/Q distributions. We compared MMIMS-derived shunt (MM-S) to Riley shunt, and MMIMS-derived dead space (MM-VD) to Bohr dead space in 349 data pairs. MM-S was on average lower than Riley shunt (- 0.05 ± 0.10), with lower and upper limits of agreement of - 0.15 and 0.04, respectively. MM-VD was on average lower than Bohr dead space (- 0.09 ± 0.14), with lower and upper limits of agreement of - 0.24 and 0.05. MM-S and MM-VD correlated and agreed well with Riley shunt and with Bohr dead space. MM-S increased significantly after lung injury only in the lavage group, whereas MM-VD increased significantly in both groups. This is the first work evaluating and demonstrating the feasibility of near real-time VA/Q distribution measurements with the MIGET and the MMIMS methods.

Dead space in acute respiratory distress syndrome.

Dead space is the portion of each tidal volume that does not take part in gas exchange and represents a good global index of the efficiency of the lung function. Dead space is not routinely measured in critical care practice, because the difficulties in in interpreting capnograms and the different methods of calculations. Different dead space indices can provide useful information in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) patients, where changes in microvasculature are the main determinants for the increase in dead space and consequently a worsening of the outcome. Lung recruitment is a dynamic process that combines recruitment manoeuvres (RMs) with positive end expiratory pressure (PEEP) and low Vt to recruit collapsed alveoli. Dead space guided recruitment allows avoiding regional overdistension or reduction in cardiac output in critical care patients with ALI or ARDS. Different patterns of ventilation affect also CO2 elimination; in fact, end-inspiratory pause prolongation reduces dead space, increasing respiratory system compliance; plateau pressure and consequently driving pressure increase accordingly. Dead space measurement is a reliable method that provides important clinical and prognostic information. Different capnographic indices can be useful to evaluate therapeutic interventions or setting mechanical ventilation.

Volume capnography: A narrative review

Volume capnography is the graph of expired carbon dioxide concentration against the expired volume. It often requires special and bulky equipment to be recorded. It can be used to estimate the dead space with fair amount of precision. Various formulae and equations have been described to estimate the dead space. While the Bohr formula is likely the most accurate for measurement of dead space, the Enghoff's equation is likely the most popular and convenient to use. Volume capnography has found uses in both the operating room (OR) and the Intensive Care Unit setting. It can be used to identify the optimal level of positive end-expiratory pressure in patients suffering from the acute respiratory distress syndrome as well as to identify its effect on the ventilation. In the OR, it can be invaluable to monitor ventilation and alveolar recruitment in the obese population. It is also a useful diagnostic adjunct in medical emergencies like pulmonary embolism. In the pediatric population, it finds uses in the monitoring of infants suffering from bronchiolitis. In spite of its multiple and diverse uses, it remains an underutilized technology; the main reasons for this being lack of experience of the providers with volume capnography and the expensive and bulky equipment that is often required. However, volume capnography has a great deal of potential and with further advances in technology, is likely to gain popularity.

Volumetric capnography: lessons from the past and current clinical applications.

Dead space is an important component of ventilation–perfusion abnormalities. Measurement of dead space has diagnostic, prognostic and therapeutic applications. In the intensive care unit (ICU) dead space measurement can be used to guide therapy for patients with acute respiratory distress syndrome (ARDS); in the emergency department it can guide thrombolytic therapy for pulmonary embolism; in peri-operative patients it can indicate the success of recruitment maneuvers. A newly available technique called volumetric capnography (Vcap) allows measurement of physiological and alveolar dead space on a regular basis at the bedside. We discuss the components of dead space, explain important differences between the Bohr and Enghoff approaches, discuss the clinical significance of arterial to end-tidal CO2 gradient and finally summarize potential clinical indications for Vcap measurements in the emergency room, operating room and ICU.

The Effect of mechanical resistive loading on optimal respiratory signals and breathing patterns under added dead space and CO2 breathing

Current study aims to investigate how the respiratory resistive loading affects the behaviour of the optimal chemical-mechanical respiratory control model, the respiratory signals and breathing pattern are optimized under external dead space loading and CO2 breathing. The respiratory control was modelled to include a neuro-muscular drive as the control output to derive the waveshapes of instantaneous airflow, lung volume profiles, and breathing pattern, including total/alveolar ventilation, breathing frequency, tidal volume, inspiratory/expiratory duration, duty cycle, and arterial CO2 pressure. The simulations were performed under various respiratory resistive loads, including no load, inspiratory resistive load, expiratory resistive load, and continuous resistive load. The dead space measurement was described with Gray’s derivation, and simulation results were studied and compared with experimental findings.

Monitoring Dead Space in Mechanically Ventilated Children: Volumetric Capnography Versus Time-Based Capnography.

Volumetric capnography dead-space measurements (physiologic dead-space-to-tidal-volume ratio [VD/VT] and alveolar VD/VT) are considered more accurate than the more readily available time-based capnography dead-space measurement (end-tidal alveolar dead-space fraction [AVDSF]). We sought to investigate the correlation between volumetric capnography and time-based capnography dead-space measurements. This was a single-center prospective cohort study of 65 mechanically ventilated children with arterial lines. Physiologic VD/VT, alveolar VD/VT, and AVDSF were calculated with each arterial blood gas using capnography data. We analyzed 534 arterial blood gases from 65 children (median age 4.9 y, interquartile range 1.7-12.8). The correlation between physiologic VD/VT and AVDSF (r = 0.66, 95% CI 0.59-0.72) was weaker than the correlation between alveolar VD/VT and AVDSF (r = 0.8, 95% CI 0.76-0.85). The correlation between physiologic VD/VT and AVDSF was weaker in children with low PaO2 /FIO2 (< 200 mm Hg), low exhaled VT (< 100 mL), a pulmonary reason for mechanical ventilation, or large airway VD (> 3 mL/kg). All 3 dead-space measurements were highly correlated (r > 0.7) in children without hypoxemia (PaO2 /FIO2 > 300 mm Hg), mechanically ventilated for a neurologic or cardiac reason, or on significant inotropes or vasopressors. In mechanically ventilated children without significant hypoxemia or with cardiac output-related dead-space changes, physiologic VD/VT was highly correlated with AVDSF and alveolar VD/VT. In children with significant hypoxemia, physiologic VD/VT was poorly correlated with AVDSF. Alveolar VD/VT and AVDSF correlated well in most tested circumstances. Therefore, AVDSF may be useful in most children for alveolar dead-space monitoring.

Effect of body position on ventilation distribution during PEEP titration in a porcine model of acute lung injury using advanced respiratory monitoring and electrical impedance tomography.

BackgroundLung failure after acute lung injury remains a challenge in different clinical settings. Various interventions for restoration of gas exchange have been investigated. Recruitment of collapsed alveoli by positive end expiratory pressure (PEEP) titration and optimization of ventilation-perfusion ratio by prone positioning have been extensively described in animal and clinical trials. This animal study was conducted to investigate the effects of PEEP and positioning by means of advanced respiratory monitoring including gas exchange, respiratory mechanics, volumetric capnography and electrical impedance tomography.MethodsAfter induction of acute lung injury by oleic acid and lung lavage, 12 domestic pigs were studied in randomly assigned supine or prone position during a PEEP titration trial with maximal PEEP of 30 mbar.ResultsInduction of lung injury resulted in significant deterioration of oxygenation [partial pressure of arterial oxygen/inspiratory fraction of oxygen (PaO2/FiO2): p = 0.002] and ventilation [partial pressure of arterial carbon dioxide (PaCO2): p = 0.002] and elevated alveolar dead-space ratios (Valv/Vte: p = 0.003) in both groups. Differences in the prone and the supine group were significant for PaCO2 at incremental PEEP 10 and 20 and at decremental PEEP 20 (20d) and 10 (10d), for PaO2/FiO2 at PEEP 10 and 10d and for alveolar dead space at PEEP 10d. Electrical impedance tomography revealed homogenous ventilation distribution in prone position during PEEP 20, 30 and 20d.ConclusionsProne position leads to improved oxygenation and ventilation parameters in a lung injury model. Respiratory monitoring with measurement of alveolar dead space and electrical impedance tomography may visualize optimized ventilation in a PEEP titration trial.

Dead space: the physiology of wasted ventilation.

An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V'A/Q') heterogeneity has been the most important pathophysiological mechanism. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V'A/Q' ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.

OPTIMAL RESPIRATORY CONTROL SIMULATION AND COMPARATIVE STUDY OF HYPERCAPNIC VENTILATORY RESPONSES TO EXTERNAL DEAD SPACE LOADING

There has been considerable research effort regarding ventilatory responses to breathing with an imposed external dead space, and inhalation of fixed levels of CO 2 by human subjects. A human respiratory control model incorporating the optimality hypothesis can successfully demonstrate ventilatory responses to both chemical stimuli and muscular exercise. In this study, to verify the model behavior of the optimal chemical–mechanical respiratory control model, we simulated the ventilatory control under dead space loading and CO 2 inhalation. The simulation was provided by a LabVIEW® based human respiratory control simulator and signal monitoring system. The dead space measurement was described with two distinct models, derived from Gray and Coon, and predicted behaviors with corresponding ventilatory responses were investigated and compared with experimental findings. While both dead space models produced satisfactory predictions on simulated optimal [Formula: see text] versus Pa CO 2, [Formula: see text] versus Pa CO 2, F versus PI CO 2, VT versus PI CO 2, VD-total versus VT, VD- total /VT versus VT, [Formula: see text] versus VT and [Formula: see text] versus VT relationships, Gray's model provided better correlation and more consistent results throughout most of the ventilatory responses. The study of relative behavior of respiratory signals and comparative relationship of the ventilator responses between dead space loading during rest and CO 2 inhalation will certainly provide valuable understanding of increases in central respiratory motor command output of human respiratory control, which is also associated with Dyspnea on exertion, and give potential clinical perspective to realize the impaired ability to excrete CO 2 in patients diagnosed with acute respiratory distress syndrome.

Volumetric capnography: the time has come.

Volumetric capnography (VCap) measures the kinetics of carbon dioxide (CO2) elimination on a breath-by-breath basis. A volumetric capnogram contains extensive physiological information about metabolic production, circulatory transport and CO2 elimination within the lungs. VCap is also the best clinical tool to measure dead spaces allowing a detailed analysis of the functional components of each tidal volume, thereby providing clinically useful hints about the lung's efficiency of gas exchange. Difficulties in its bedside measurement, oversimplifications of its interpretation along with prevailing misconceptions regarding dead space analysis have, however, limited its adoption as a routine tool for monitoring mechanically ventilated patients. Improvements in CO2 measuring technologies and more advanced algorithms for faster and more accurate analysis of volumetric capnograms have increased our physiological understanding and thus the clinical usefulness of VCap. The recently validated VCap-based method for estimating alveolar partial pressure of CO2 provided a breakthrough for a fully noninvasive breath-by-breath measurement of physiological dead space. Recent advances in VCap and our improved understanding of its clinical implications may help in overcoming the known limitations and reluctances to include expired CO2 kinetics and dead space analysis in routine bedside monitoring. It is about time to start using this powerful monitoring tool to support decision making in the intensive care environment.

Prediction equation to estimate dead space to tidal volume fraction correlates with mortality in critically ill patients

ObjectiveThe measurement of dead space to tidal volume fraction (Vd/Vt) using various methodologies has been shown to be a reliable predictor of mortality in critically ill patients. In this study, we evaluated the correlation of a validated equation using clinically available information to predict calculation of Vd/Vt with clinically relevant outcome parameters in patients requiring mechanical ventilation. MethodsCalculations of Vd/Vt were obtained based upon a previously published prediction equation for dead space ventilation fraction: Vd/Vt = 0.320 + 0.0106 (Paco2 − end-tidal carbon dioxide measurement) + 0.003 (respiratory rate per minute) + 0.0015 (age in years) on study days 1, 3 to 4, 6 to 9, and 14 after initiation of mechanical ventilation in adult patients who satisfied 1 of the 3 study defined diseases: (1) acute bacterial pneumonia, (2) acute respiratory distress syndrome, or (3) cystic fibrosis. ResultsUsing the final/last available time point calculation of Vd/Vt, a significant difference was observed between survivors and nonsurvivors both in relation to mean and median values (56.5% vs 71.2% and 56.0% vs 65.0%, respectively). In addition, sequential analyses of Vd/Vt calculations over time also demonstrated a statistically significant difference between survivors and nonsurvivors for days 6 to 9. ConclusionIn this study-specific population of critically ill patients, the prediction equation of Vd/Vt using clinically available parameters correlates with mortality. In addition, we provide a simple method to estimate Vd/Vt that can be potentially applicable to all critically ill intensive care unit patients.

Translational toxicological research: investigating and preventing acute lung injury in organophosphorus insecticide poisoning

Poisoning through ingestion of organophosphorus (OP) insecticide is a leading cause of suicide globally. Severe poisoning with OP compounds creates an unconscious, paralysed patient with respiratory failure. These symptoms make...

Near-real time pulmonary shunt and deadspace measurement with multiple inert gas elimination technique (MIGET) by micropore membrane inlet mass spectrometry (MMIMS) in porcine lung injury models

Near-real time pulmonary shunt and deadspace measurement with multiple inert gas elimination technique (MIGET) by micropore membrane inlet mass spectrometry (MMIMS) in porcine lung injury models

Rationale of Dead Space Measurement by Volumetric Capnography

Dead space is the portion of a tidal volume that does not participate in gas exchange because it does not get in contact with blood flowing through the pulmonary capillaries. It is commonly calculated using volumetric capnography, the plot of expired carbon dioxide (CO(2)) versus tidal volume, which is an easy bedside assessment of the inefficiency of a particular ventilatory setting. Today, Bohr's original dead space can be calculated in an entirely noninvasive and breath-by-breath manner as the mean alveolar partial pressure of CO(2) (Paco(2)) which can now be determined directly from the capnogram. The value derived from Enghoff's modification of Bohr's formula (using Paco(2) instead of PACO(2)) is a global index of the inefficiency of gas exchange rather than a true "dead space" because it is influenced by all causes of ventilation/perfusion mismatching, from real dead space to shunt. Therefore, the results obtained by Bohr's and Enghoff's formulas have different physiological meanings and clinicians must be conscious of such differences when interpreting patient data. In this article, we describe the rationale of dead space measurements by volumetric capnography and discuss its main clinical implications and the misconceptions surrounding it.

Measurement of Dead Space During Anesthesia

To the Editor Badal et al.1 were neither precise nor consistent in the terminology and abbreviations used as part of the article describing measurements of dead space during anesthesia. They state that Bohr's equation was used to calculate alveolar dead space when, in fact, Enghoff's modification of Bohr's original equation (VD/VT = PaCO2 − PECO2/PaCO2) measuring physiologic dead space (which contains alveolar dead space and airway-anatomic dead space) was used.2 Because such imprecise terminology (apparatus, anatomic, pulmonary, alveolar, physiologic) and abbreviations (VDS/VT, VDC, VDc, VD) appear throughout the text, figures, and table, it is difficult to judge the results unless one is very familiar with the subject. A second point concerns study design and results. Referencing their previous work,3 the authors acknowledge the inherent limitations of their methods providing “an accurate approximation” of mixed expired PCO2. Therefore, a randomized study with a larger, more uniform population combined with measurement of true alveolar dead space using standard mainstream volumetric capnography would provide more insights into the real clinical value of the proposed method. Third, the method is presented as simple and inexpensive. However, it requires an additional capnograph as well as significant modification of the anesthesia circuit with the potential of leakage at the entrance of the sample line into the ventilator bellows. Yves P. S. Moens, DVM Division of Anaesthesiology and perioperative Intensive Care University of Veterinary Medicine Vienna, Austria [email protected] Gerardo Tusman, MD Department of Anaesthesiology Hospital Privado de Comunidad Mar del Plata, Argentina Martina Mosing, DVM Section of Anaesthesiology Vetsuisse Faculty University of Zürich Zürich, Switzerland Stephan Böhm, MD CSEM Centre Suisse d'Electronique et de Microtechnique SA Research Centre for Nanomedicine Landquart, Switzerland

Comment on Tusman et al.: Validation of Bohr dead space measured by volumetric capnography

Dear Editor, I read with great interest the paper by Tusman et al. on Bohr dead space (VDBohr) measurement from volumetric capnography. Their analysis based on an equation fitting the CO2 expirogram provides a substantial improvement for the objective assessment of its components [1]. Even though it is clear that the use of PaCO2 as a surrogate for ideal alveolar PCO2 in the Bohr equation— as suggested by Enghoff—may lead to overestimation of physiological dead space [2, 3], replacing it for mean alveolar PCO2 (PACO2)—as originally devised by Bohr and recently accomplished by Tusman et al. [1]—will solely account for airway dead space (VDaw) and not for alveolar dead space (VDalv). This is shown by the following set of equations. According to Fowler’s approach, tidal volume (VT) divides into VDaw and alveolar VT (VTalv); VT = VDaw ? VTalv. The mixed expired CO2 fraction (FeCO2) over one breath is the ratio between the expired CO2 volume (VCO2br) and VT; FeCO2 = VCO2br/VT. According to the alveolar gas equation, the mean alveolar CO2 fraction (FACO2) is the ratio between VCO2br and VTalv, or FACO2 = VCO2br/(VT– VDaw). Replacing the terms above in the Bohr equation as suggested by Tusman et al. [1] gives:

Deadspace ventilation: a waste of breath!

Problems with ventilatory efficiency results in abnormal CO(2) clearance. Measuring deadspace ventilation should be the most reliable method of monitoring ventilatory efficiency in mechanically ventilated patients. Since its first description by Bohr in the late 19th century to the current use of single-breath test for volumetric CO(2), our understanding of the physiological deadspace has vastly improved. Yet indices of oxygenation seem to be the mainstay when instigating or fine-tuning ventilatory strategies. Deadspace and with it ventilatory efficiency has been largely forgotten. Recently though there has been a resurgence of interest in ventilatory efficiency. Several indices have been described that either predict deadspace or track ventilatory efficiency at the bedside. Thus making it more accessible and easy to monitor and study in large groups of patients, factors which have perhaps resulted in its under-utilisation in critical care. This review revisits the physiological concepts and methods of measuring deadspace. Described are the various clinical applications of deadspace measurements in the critically unwell. The potential reasons that have led to the variable being under-used are also examined. Finally we describe the indices currently available to track ventilatory efficiency at the bedside.