Monitoring CO2 kinetics as a marker of cardiopulmonary efficiency.

PURPOSE OF REVIEW: To describe current and near future developments and applications of CO2 kinetics in clinical respiratory and cardiovascular monitoring. RECENT FINDINGS: In the last years, we have witnessed a renewed interest in CO2 kinetics in relation with a better understanding of volumetric capnography and its derived parameters. This together with technological advances and improved measurement systems have expanded the monitoring potential of CO2 kinetics including breath by breath continuous end-expiratory lung volume and continuous noninvasive cardiac output. Dead space has slowly been gaining relevance in clinical monitoring and prognostic evaluation. Easy to measure dead space surrogates such as the ventilatory ratio have demonstrated a strong prognostic value in patients with acute respiratory failure. SUMMARY: The kinetics of carbon dioxide describe many relevant physiological processes. The clinical introduction of new ways of assessing respiratory and circulatory efficiency based on advanced analysis of CO2 kinetics are paving the road to a long-desired goal in clinical monitoring of critically ill patients: the integration of respiratory and circulatory monitoring during mechanical ventilation.

Large animal ventilator-integrated volumetric capnography generates clinically acceptable values of physiologic dead space in anesthetized healthy adult horses.

OBJECTIVE: To evaluate the agreement between the Tafonius large animal ventilator-integrated volumetric capnography (vCap) software and the Respironics NICO noninvasive cardiac output monitor reference system. ANIMALS: Data were collected from 56 healthy adult horses undergoing general anesthesia. METHODS: Animals were placed under general anesthesia and connected to the Tafonius large animal ventilator circle system. A flow partitioning device with CO2 and flow sensors was utilized to couple the endotracheal tube to the NICO monitor. Tafonius CO2 and flow sensors are incorporated into the Y-piece of the breathing circuit. Arterial blood samples were collected to determine the partial pressure of arterial carbon dioxide (PaCO2) immediately before data collection. The PaCO2 was input into the Tafonius and NICO monitor, and dead space ventilation (%Vd), end-tidal CO2 partial pressure (ETco2), mixed-expired CO2 partial pressure (Peco2), and expired tidal volume (Vt) were calculated over a single breath. Multiple measurements were completed for each patient, with a total of 200 paired data points collected for analysis. Data were assessed for normality, and Bland-Altman analysis was performed. Bias and 95% limits of agreement were calculated. RESULTS: The limits of agreement for %Vd of the ventilator-derived measurements fell within ± 10% of the NICO monitor reference method. CLINICAL RELEVANCE: Our results indicate that, when compared to the NICO monitor method, the Tafonius-integrated vCap software provides clinically acceptable values of Peco2, Vt, and %Vd in healthy adult horses.

SAMAY S24: a novel wireless 'online' device for real-time monitoring and analysis of volumetric capnography.

Volumetric capnography (VCap) provides information about CO2 exhaled per breath (VCO2br) and physiologic dead space (VDphys). A novel wireless device with a high response time CO2 mainstream sensor coupled with a digital flowmeter was designed to monitor all VCap parameters online in rabbits (SAMAY S24).Ten New Zealand rabbits were anesthetized and mechanically ventilated. VCO2br corresponds to the area under the VCap curve. We used the modified Langley method to assess the airway VD (VDaw) and the alveolar CO2 pressure. VDphys was estimated using Bohr's formula, and the alveolar VD was calculated by subtracting VDaw from VDphys. We compared (Bland-Altman) the critical VCap parameters obtained by SAMAY S24 (Langley) with the Functional Approximation based on the Levenberg-Marquardt Algorithm (FA-LMA) approach during closed and opened chest conditions.SAMAY S24 could assess dead space volumes and VCap shape in real time with similar accuracy and precision compared to the 'offline' FA-LMA approach. The opened chest condition impaired CO2 kinetics, decreasing the phase II slope, which was correlated with the volume of CO2 exhaled per minute.

A coupled model for the dynamics of gas exchanges in the human lung with Haldane and Bohr's effects.

We propose an integrated dynamical model for oxygen and carbon dioxide transfer from the lung into the blood, coupled with a lumped mechanical model for the ventilation process, for healthy patients as well as in pathological cases. In particular, we take into account the nonlinear interaction between oxygen and carbon dioxide in the blood volume, referred to as the Bohr and Haldane effects. We also propose a definition of the physiological dead space volume (the lung volume that does not contribute to gas exchange) which depends on the pathological state and the breathing scenario. This coupled ventilation-gas diffusion model is driven by the sole action of the respiratory muscles. We analyse its sensitivity with respect to characteristic parameters: the resistance of the bronchial tree, the elastance of the lung tissue and the oxygen and carbon dioxide diffusion coefficients of the alveolo-capillary membrane. Idealized pathological situations are also numerically investigated. We obtain realistic qualitative tendencies, which represent a first step towards classification of the pathological behaviours with respect to the considered input parameters.

Effect of external dead space removal on CO2 homeostasis in mechanically ventilated adult Covid-19 patients.

BACKGROUND: Patients with Covid-19 respiratory failure present with hypoxemia, often in combination with hypercapnia. In this prospective, observational study we examined the effect of removing external dead space (DS) on CO2 -homeostasis in mechanically ventilated Covid-19 patients. In addition, volumetric capnography was validated for its ability to estimate external DS volume using in vitro measured DS volumes as reference. METHODS: In total, 10 patients with acute respiratory distress syndrome from Covid-19 were included. Volumetric capnography, mechanical ventilation, and arterial blood gas data were analyzed before and after removal of external DS and analyzed for potentially significant changes in response to DS removal. Measurements of external DS were obtained in circuit using volumetric capnography and compared to actual measured DS volumes off the circuit. RESULTS: After the removal of external DS, the alveolar minute ventilation and CO2 elimination improved, notwithstanding unchanged respiratory rate and tidal volumes. The increase in CO2 elimination was associated with a decrease in arterial CO2 partial pressure (PaCO2 ). The volumetric capnography method for assessment of external DS showed a low bias of -9 mL (lower limit of agreement -40, 95% CI -60 to -20 mL, upper limit of agreement 21 mL, 95% CI: 1-40 mL) and a percentage error of 48% compared to absolute values measured in vitro. CONCLUSION: Removal of external DS increased alveolar minute ventilation and CO2 elimination in Covid-19 patients with respiratory failure in the current study. This was associated with a decrease in PaCO2 . This may indicate a decreased CO2 production due to decreased work of breathing and more effective gas-exchange in response to DS removal. In addition, volumetric capnography appears to be a clinically feasible method for continuous measurement of external DS in the current study and may be of value in optimizing ventilator treatment.

Alveolar target ventilation and dead space in children under anaesthesia: The proventiped cohort study.

INTRODUCTION: Ventilator settings in children under anaesthesia remain difficult because of the changes in the physiology and the high dead space. OBJECTIVE: To determine the alveolar minute-volume to sustain normocapnia in children under mechanical ventilation. DESIGN: A prospective observational study. SETTINGS: This study was performed between May and October 2019 in a tertiary care children's hospital. PATIENTS: Children between 2 months and 12 years, weighing between 5 and 40 kg, admitted for general anaesthesia. INTERVENTION: Volumetric capnography was used to estimate the alveolar and dead space volume (Vd). MAIN OUTCOME MEASURES: Total and alveolar minute ventilation in (ml kg -1  min -1 ) over 100 breaths. RESULTS: Sixty patients were included comprising 20 per group: 5 to 10 kg (group 1), 10 to 20 kg (group 2), 20 to 40 kg (group 3). Seven patients were excluded for aberrant capnographic curves. After normalisation to weight, the median [IQR] tidal volume per kilogram was similar between the three groups: 6.5 ml kg -1 [6.0 to 7.5 ml kg -1 ], 6.4  ml kg -1 [5.7 to 7.3  ml kg -1 ], 6.4  ml kg -1 [5.3 to 6.8  ml kg -1 ]; P  = 0.3. Total Vd (in ml kg -1 ) was negatively correlated to weight ( r  = -0.62, 95% confidence interval -0.41 to -0.76, P  < 0.001). The total normalised minute ventilation (ml kg -1  min -1 ) to obtain normocapnia was higher in group 1 than in group 2 and in group 3; 203  ml kg -1  min -1 [175 to 219 ml kg -1  min -1 ], 150  ml kg -1  min -1 [139 to 181  ml kg -1  min -1 ] and 128  ml kg -1  min -1 [107 to 157  ml kg -1  min -1 ]; P  < 0.001 (mean ± SD), but (mean ± SD) alveolar minute ventilation was similar between the three groups; 68 ±â€Š21  ml kg -1  min -1 . CONCLUSION: Total dead space volume (including apparatus dead space) represents a major component of tidal volume in children less than 30 kg, when using large heat and moisture exchanger filters. The total minute ventilation necessary to achieve normocapnia decreased with increasing weight, while the alveolar minute ventilation remained constant. TRIAL REGISTRATION: ClinicalTrials.gov, identifier: NCT03901599.

Dead space ventilation-related indices: bedside tools to evaluate the ventilation and perfusion relationship in patients with acute respiratory distress syndrome.

Cumulative evidence has demonstrated that the ventilatory ratio closely correlates with mortality in acute respiratory distress syndrome (ARDS), and a primary feature in coronavirus disease 2019 (COVID-19)-ARDS is increased dead space that has been reported recently. Thus, new attention has been given to this group of dead space ventilation-related indices, such as physiological dead space fraction, ventilatory ratio, and end-tidal-to-arterial PCO2 ratio, which, albeit distinctive, are all global indices with which to assess the relationship between ventilation and perfusion. These parameters have already been applied to positive end expiratory pressure titration, prediction of responses to the prone position and the field of extracorporeal life support for patients suffering from ARDS. Dead space ventilation-related indices remain hampered by several deflects; notwithstanding, for this catastrophic syndrome, they may facilitate better stratifications and identifications of subphenotypes, thereby providing therapy tailored to individual needs.

[Dead space fraction for treatment guidance and prognosis evaluation of acute respiratory distress syndrome].

Acute respiratory distress syndrome (ARDS) is a common cause of critical illness and high mortality from respiratory failure. Increased dead space fraction (VD/VT) was independently associated with lung injury and mortality of ARDS. VD/VT is readily obtained by bedside measurements of arterial blood gas and end-tidal carbon dioxide. Early attention and application of VD/VT as an indicator will help to better understand the pathophysiological of ARDS, guide clinical treatment, and better assess the severity and clinical prognosis of the disease.

Alveolar Dead Space Is Augmented During Exercise in Patients With Heart Failure With Preserved Ejection Fraction.

BACKGROUND: Patients with heart failure with preserved ejection fraction (HFpEF) exhibit many cardiopulmonary abnormalities that could result in V˙/Q˙ mismatch, manifesting as an increase in alveolar dead space (VDalveolar) during exercise. Therefore, we tested the hypothesis that VDalveolar would increase during exercise to a greater extent in patients with HFpEF compared with control participants. RESEARCH QUESTION: Do patients with HFpEF develop VDalveolar during exercise? STUDY DESIGN AND METHODS: Twenty-three patients with HFpEF and 12 control participants were studied. Gas exchange (ventilation [V˙E], oxygen uptake [V˙o2], and CO2 elimination [V˙co2]) and arterial blood gases were analyzed at rest, twenty watts (20W), and peak exercise. Ventilatory efficiency (evaluated as the V˙E/V˙co2 slope) also was measured from rest to 20W in patients with HFpEF. The physiologic dead space (VDphysiologic) to tidal volume (VT) ratio (VD/VT) was calculated using the Enghoff modification of the Bohr equation. VDalveolar was calculated as: (VD / VT × VT) - anatomic dead space. Data were analyzed between groups (patients with HFpEF vs control participants) across conditions (rest, 20W, and peak exercise) using a two-way repeated measures analysis of variance and relationships were analyzed using Pearson correlation coefficient. RESULTS: VDalveolar increased from rest (0.12 ± 0.07 L/breath) to 20W (0.22 ± 0.08 L/breath) in patients with HFpEF (P < .01), whereas VDalveolar did not change from rest (0.01 ± 0.06 L/breath) to 20W (0.06 ± 0.13 L/breath) in control participants (P = .19). Thereafter, VDalveolar increased from 20W to peak exercise in patients with HFpEF (0.37 ± 0.16 L/breath; P < .01 vs 20W) and control participants (0.19 ± 0.17 L/breath; P = .03 vs 20W). VDalveolar was greater in patients with HFpEF compared with control participants at rest, 20W, and peak exercise (main effect for group, P < .01). Moreover, the increase in VDalveolar correlated with the V˙E/V˙co2 slope (r = 0.69; P < .01), which was correlated with peak V˙o2peak (r = 0.46; P < .01) in patients with HFpEF. INTERPRETATION: These data suggest that the increase in V˙/Q˙ mismatch may be explained by increases in VDalveolar and that increases in VDalveolar worsens ventilatory efficiency, which seems to be a key contributor to exercise intolerance in patients with HFpEF.

Increased respiratory dead space could associate with coagulation activation and poor outcomes in COVID-19 ARDS.

PURPOSE: To determine whether VDPhys/VT is associated with coagulation activation and outcomes. MATERIALS AND METHODS: We enrolled patients with COVID-19 pneumonia who were supported by invasive mechanical ventilation and were monitored using volumetric capnography. Measurements were performed during the first 24 h of mechanical ventilation. The primary endpoint was the likelihood of being discharge alive on day 28. RESULTS: Sixty patients were enrolled, of which 25 (42%) had high VDPhys/VT (>57%). Patients with high vs. low VDPhys/VT had higher APACHE II (10[8-13] vs. 8[6-9] points, p = 0.002), lower static compliance of the respiratory system (35[24-46] mL/cmH2O vs. 42[37-45] mL/cmH2O, p = 0.005), and higher D-dimer levels (1246[1050-1594] ng FEU/mL vs. 792[538-1159] ng FEU/mL, p = 0.001), without differences in P/F ratio (157[112-226] vs. 168[136-226], p = 0.719). Additionally, D-dimer levels correlated with VDPhys/VT (r = 0.530, p < 0.001), but not with the P/F ratio (r = -0.103, p = 0.433). Patients with high VDPhys/VT were less likely to be discharged alive on day 28 (32% vs. 71%, aHR = 3.393[1.161-9.915], p = 0.026). CONCLUSIONS: In critically ill COVID-19 patients, increased VDPhys/VT was associated with high D-dimer levels and a lower likelihood of being discharged alive. Dichotomic VDPhys/VT could help identify a high-risk subgroup of patients neglected by the P/F ratio.

Dead space washout by intentional leakage flow during conventional ventilation of premature infants-an experimental study.

OBJECTIVE: Invasive mechanical ventilation poses a strong risk factor for the development of chronic lung disease in preterm infants. A reduction of the dead space as part of the total breathing volume would reduce the ventilation effort and thereby lower the risk of ventilator-induced lung injuries. In this experimental study, we compared the efficacy of mechanical dead space washout via uncontrolled and controlled leakage flow in their ability to eliminate CO2 during conventional ventilation in preterm infants. METHODS: Three frequently used neonatal ventilators, operating under standard conventional ventilating parameters, were individually connected to a test lung. To maintain a constant physiological end-expiratory pCO2 level during ventilation, the test lung was continuously flooded with CO2 . A side port in the area of the connector between the endotracheal tube and the flow sensor allowed breathing gas to escape passively or in a second experimental setup, regulated by a pump. Measurements of end-expiratory pCO2 were taken in both experiments and compared to end-expiratory pCO2 levels of ventilation without active dead space leakage. RESULTS: Following dead space washout, a significant reduction of end-expiratory pCO2 was attained. Under conditions of uncontrolled leakage, the mean decrease was 14.1% while controlled leakage saw a mean reduction of 16.1%. CONCLUSION: Washout of dead space by way of leakage flow is an effective method to reduce end-expiratory pCO2 . Both controlled and uncontrolled leakage provide comparable results, but precise regulation of leakage allows for a more stable ventilation by preventing uncontrolled loss of tidal volume during inspiration.

Exercise Tolerance in Patients With Idiopathic Pulmonary Fibrosis, Effect of Supplemental Oxy-Gen.

Exercise tolerance in patients with idiopathic pulmonary fibrosis IPF is mainly limited by mechanical constrain of ventilation and high physiologic dead space. Oxygen enriched gas inhalation seems to increase ventilatory efficiency by reduction of dead space to tidal volume ratio (VD/VT) which probably mirrors improved pulmonary capillary flow and leads to longer physical tolerance at lower level of minute ventilation. The effect is noticeable at FIO2 that can be delivered in rehabilitation purposes or daily living activities.

Physiological dead space during exercise in patients with heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) is associated with cardiopulmonary abnormalities that may increase physiological dead space to tidal volume (VD/VT) during exercise. However, studies have not corrected VD/VT for apparatus mechanical dead space (VDM), which may confound the accurate calculation of VD/VT. We evaluated whether calculating physiological dead space with (VD/VTVDM) and without (VD/VT) correcting for VDM impacts the interpretation of gas exchange efficiency during exercise in HFpEF. Fifteen HFpEF (age: 69 ± 6 yr; V̇o2peak: 1.34 ± 0.45 L/min) and 12 controls (70 ± 3 yr; V̇o2peak: 1.70 ± 0.51 L/min) were studied. Pulmonary gas exchange and arterial blood gases were analyzed at rest, submaximal (20 W for HFpEF and 40 W for controls), and peak exercise. VD/VT was calculated as [Formula: see text] - [Formula: see text]/[Formula: see text]. VD/VTVDM was calculated as [Formula: see text] - [Formula: see text]/[Formula: see text] - VDM/VT. VD/VT decreased from rest (HFpEF: 0.54 ± 0.07; controls: 0.32 ± 0.07) to submaximal exercise (HFpEF: 0.46 ± 0.07; controls: 0.25 ± 0.06) in both groups (P < 0.05), but remained stable (P > 0.05) thereafter to peak exercise (HFpEF: 0.46 ± 0.09; controls: 0.22 ± 0.05). In HFpEF, VD/VTVDM did not change (P = 0.58) from rest (0.29 ± 0.07) to submaximal exercise (0.29 ± 0.06), but increased (P = 0.02) thereafter to peak exercise (0.33 ± 0.06). In controls, VD/VTVDM remained stable such that no change was observed (P > 0.05) from rest (0.17 ± 0.06) to submaximal exercise (0.14 ± 0.06), or thereafter to peak exercise (0.14 ± 0.05). Calculating physiological dead space with and without a VDM correction yields quantitively and qualitatively different results, which could have impact on the interpretation of gas exchange efficiency in HFpEF. Further investigation is required to uncover the clinical consequences and the mechanism(s) explaining the increase in VD/VTVDM during exercise in HFpEF.NEW & NOTEWORTHY Calculating VD/VT with and without correcting for VDM yields quantitively and qualitatively different results, which could have an important impact on the interpretation of V/Q mismatch in HFpEF. The finding that V/Q mismatch and gas exchange efficiency worsened, as reflected by an increase in VD/VTVDM during exercise, has not been previously demonstrated in HFpEF. Thus, further studies are needed to investigate the mechanisms explaining the increase in VD/VTVDM during exercise in patients with HFpEF.

El espacio muerto (VD/VT) como predictor de éxito en la extubación de pacientes postquirúrgicos de cirugía cardiovascular pediátrica / Dead space (VD/VT) as a predictor of successful extubation of patients after pediatric cardiovascular surgery

Introducción: La ventilación mecánica (VM) forma parte de la recuperación postoperatoria (PO) de niños con cirugía de cardiopatía congénita, pero su uso no está exento de riesgos. El fracaso de extubación (FE) se ha asociado con internaciones prolongadas, aumento de complicaciones y mortalidad. El objetivo es determinar un valor de Vd/Vt predictor de extubación exitosa (EE). Material y métodos: estudio de cohorte prospectivo y observacional realizado del 1 de Enero al 31 de Diciembre de 2016 en niños menores de 6 meses cursando PO de cirugía cardiovascular con circulación extracorpórea (CEC) con requerimientos de VM por más de 48 horas. En los mismo se analizó el éxito o fracaso de extubación. Previo a la extubación se registraron valores de mecánica respiratoria; Vd/Vt, CO2 espiratoria final, Vt/kg, etc. Otras variables registradas: edad, sexo, peso, requerimiento de VM antes de la cirugía, fisiología de ventrículo único, duración de VM, complicaciones, duración de la internación y mortalidad. Las variables continuas se describieron como mediana y rango intercuartilo (25-75) y se compararon con prueba de Wilcoxon, las categóricas como proporciones o porcentajes y se analizaron con chi2 . Se efectuó un análisis bivariado con diferentes puntos de corte de Vd/Vt pre extubación para realizar un análisis de sensibilidad del valor predictivo de EE. Resultados: Se evaluó Vd/Vt en 67 pacientes, tres se eliminaron por parálisis cordal (1) y parálisis del diafragma (2). Mediana de edad 23 días (10-55), peso 3.2 Kg (2.89- 3.88), días de VM 5 (3-7), días de internación 15 (2- 128), mortalidad 7,8%. Se extubaron con éxito 76% de los pacientes (50/64). Las características demográficas de los pacientes, la mecánica respiratoria, gases de sangre arterial y EtCO2 no tuvieron asociación significativa con EE. Un Vd/Vt pre extubación < 0,53 se asoció con EE. Conclusión: En la población estudiada un valor de Vd/Vt <0,53 se asoció con EE. Los pacientes con ventrículo único presentaron mayor FE.(AU)

Introduction: Mechanical ventilation (MV) is part of postoperative (PO) recovery of children with congenital heart disease surgery, but is not without risks. Extubation failure (EF) has been associated with prolonged hospital stays and increased complication and mortality rates. The goal is to determine the value of Vd/Vt as a predictor of successful extubation (SE). Material and methods: A prospective and observational cohort study was conducted from January 1 to December 31, 2016, in children under 6 months of age undergoing cardiovascular surgery with extracorporeal circulation (ECC) and requiring MV for more than 48 hours. Intubation success or failure was evaluated. Prior to extubation, respiratory mechanics values, such as Vd/Vt, final expiratory CO2, and Vt/kg, were recorded. Other variables, including age, sex, weight, VM requirement before surgery, single ventricle physiology, VM duration, complications, length of hospital stay, and mortality were also recorded. Continuous variables were described as median and interquartile range (25-75) and compared with the Wilcoxon test. Categorical variables were described as proportions or percentages and analyzed with chi2. Bivariate analysis was performed with different pre-extubation Vd/Vt cut-off points to analyze the sensitivity of the predictive value for SE. Results: Vd/Vt was evaluated in 67 patients; three were excluded because of vocal fold (1) and diaphragm paralysis (2). Median age was 23 days (10-55), weight 3.2 Kg (2.89- 3.88), days on MV 5 (3-7), length of hospital stay 15 (2- 128), and mortality rate 7.8%. Overall, 76% of patients (50/64) were successfully extubated. Patient demographics, respiratory mechanics, arterial blood gases, and EtCO2 were not significantly associated with SE. A pre-extubation Vd/ Vt < 0.53 was associated with SE. Conclusion: In this series of patients, a Vd/Vt value of <0.53 was associated with SE. EF was increased in patients with a single ventricle (AU)

Effects of Swimming with Added Respiratory Dead Space on Cardiorespiratory Fitness and Lipid Metabolism.

The aim of this study was to investigate the circulatory, respiratory, and metabolic effects of induced hypercapnia via added respiratory dead space (ARDS) during moderate-intensity swimming in recreational swimmers. A mixed-sex sample of 22 individuals was divided into homogeneous experimental (E) and control (C) groups controlled for maximal oxygen uptake (VO2max). The intervention involved 50 min of front crawl swimming performed at 60% VO2max twice weekly for 6 consecutive weeks. ARDS was induced via tube breathing (1000 ml) in group E. An incremental exercise test was administered pre- and post-intervention to assess cardiorespiratory fitness (CRF) by measuring VO2max, carbon dioxide volume, respiratory minute ventilation, respiratory exchange ratio (RER), and heart rate at 50, 100, 150, 200 W and at maximal workload. Body mass index (BMI), fat mass (FM), and fat-free mass (FFM) were also measured. The mean difference in glycerol concentration (ΔGLY) was assessed after the first and last swimming session. No significant between-group differences were observed at post-intervention. No within-group differences were observed at post-intervention except for RER which increased in group E at maximal workload. A 6-week swimming intervention with ARDS did not enhance CRF. The RER increase in group E is not indicative of a substrate shift towards increased lipid utilization. No change in ΔGLY is evident of a lack of enhanced triglyceride hydrolyzation that was also confirmed by similar pre- and post-intervention BMI, FM, and FMM.

The combined use of end-tidal carbon dioxide and alveolar dead space fraction values in the diagnosis of pulmonary embolism.

BACKGROUND: Several studies have reported that computed tomography pulmonary angiography is the best method for diagnosing pulmonary embolism (PE). This study, however, aimed to predict or exclude PE using the end-tidal carbon dioxide (ETCO2) value and alveolar dead space fraction (AVDSf) together. METHODS AND MATERIALS: One-hundred patients were included in the present study. Patients with suspected PE were evaluated using clinical prediction rules proposed by the Wells and the Modified Geneva scoring systems. PE was ruled out in patients with normal d-dimer concentrations (< 0.55 mg/dl). Patient ETCO2 values were recorded using time versus waveform capnography before performing imaging studies. Capnography was performed for 2 min; however, the average ETCO2 values measured over the final 1 min were recorded in "full continuous" mode. Arterial puncture was performed simultaneously for arterial blood gas analysis. Additionally, AVDSf was calculated according to the Bohr equation. RESULTS: PE was detected in 36 % of patients. Patients were classified into high-, moderate, and low-risk groups according to the Wells and Modified Geneva scores. PE was excluded in 95 % and 100 % of patients with low Wells and Modified Geneva system scores, respectively, when ETCO2 was > 28.5 mmHg. The diagnosis of PE was excluded in 100 % of patients with low Wells and Modified Geneva scoring system scores with AVDSf < 0.128. High wells and Modified Geneva system scores were helpful in diagnosing of PE (100 %) when AVDSf was > 0.128. CONCLUSION: It was possible to exclude/predict PE based on ETCO2 and AVDSf values calculated using capnography when evaluated with clinical prediction rules and d-dimer test using an algorithm.

Analysis of Oxygenation in Chronic Thromboembolic Pulmonary Hypertension Using Dead Space Ratio and Intrapulmonary Shunt Ratio.

Current therapeutic methods for chronic thromboembolic pulmonary hypertension (CTEPH) can improve hemodynamic status and are expected to improve prognoses. However, some patients experience dyspnea during effort and continue supplemental oxygenation despite their hemodynamic status being fully improved. Considering the pathogenesis of CTEPH, the dead space and intrapulmonary shunt are assumed to be responsible for hypoxia in CTEPH, but their contributions are unclear. It is also unclear whether they are improved after treatment. The aim of this study was to investigate the implications of the dead space ratio (DSR) and the intrapulmonary shunt ratio (ISR) for hypoxia in CTEPH and treatment for CTEPH.We retrospectively measured the DSR and ISR of 23 consecutive patients with CTEPH. For 11 of these 23 (10 were treated by balloon pulmonary angioplasty, one with riociguat), we also measured these parameters before and after CTEPH treatments. Overall, the DSR and ISR were abnormally elevated (DSR: 0.63 ± 0.06; ISR: 0.20 ± 0.05). After treatment, mean pulmonary artery pressure was improved (from 40.3 ± 8.1 to 25.5 ± 2.7 mmHg). Although atrial oxygen saturation (SaO2), DSR and ISR were improved (SaO2: from 90.2 ± 3.2 to 93.7 ± 1.8%; DSR: from 0.64 ± 0.06 to 0.58 ± 0.05; ISR: from 0.20 ± 0.04 to 0.18 ± 0.02), these improvements were slight compared with that of mean pulmonary artery pressure.The DSR and ISR were abnormally elevated in patients with CTEPH and their improvement by treatment was limited. Only DSR can be a useful marker for normalization of hypoxia in CTEPH.

Pulmonary Dead Space Monitoring: Identifying Subjects With ARDS at Risk of Developing Right Ventricular Dysfunction.

BACKGROUND: ARDS is a highly morbid condition characterized by diffuse pulmonary inflammation, which results in hypoxemic respiratory failure. Approximately 25% of patients with ARDS develop right ventricular dysfunction, with cor pulmonale being a common final pathway in a significant number of non-survivors. ARDS-related right ventricular dysfunction occurs due to acute elevation in ventricular afterload caused by mechanisms that are associated with increased pulmonary dead space fraction. Thus, we hypothesized that changes in pulmonary dead space fraction may reflect changes in pulmonary hemodynamics. METHODS: This was a prospective single-center study of 21 subjects with ARDS who underwent serial determination of pulmonary dead space fraction and pulmonary hemodynamics via transthoracic echocardiography. Linear mixed-effects modeling was performed to test for an association between a change in pulmonary dead space and a change in pulmonary hemodynamics. RESULTS: The tricuspid regurgitation velocity to right ventricular outflow track velocity time integral ratio, an echocardiographic surrogate for pulmonary vascular resistance, increased by 0.16 Wood units (Coefficient 0.16, 95% CI 0.09-0.23; P < .001), and the tricuspid regurgitation pressure gradient increased by 3.7 mm Hg (Coefficient 3.7, 95% CI 1.74-5.63, P < .001) for every 10% increase in pulmonary dead space fraction. CONCLUSIONS: Increases in the pulmonary dead space fraction were associated with relative increases in both the tricuspid regurgitation velocity to right ventricular outflow track velocity time integral ratio and the tricuspid regurgitation pressure gradient, which likely contributed to the high incidence of ARDS-related right ventricular dysfunction encountered in clinical practice. Pulmonary dead space monitoring may serve as a clinical indicator to identify patients with ARDS at risk of developing right ventricular dysfunction and acute cor pulmonale.