Physiological Dead Space Research Articles

Transcutaneous PCO2 for Exercise Gas Exchange Efficiency in Chronic Obstructive Pulmonary Disease

Gas exchange inefficiency and dynamic hyperinflation contributes to exercise limitation in chronic obstructive pulmonary disease (COPD). It is also characterized by an elevated fraction of physiological dead space (VD/VT). Noninvasive methods for accurate VD/VT assessment during exercise in patients are lacking. The current study sought to compare transcutaneous PCO2 (TcPCO2) with the gold standard—arterial PCO2 (PaCO2)—and other available methods (end tidal CO2 and the Jones equation) for estimating VD/VT during incremental exercise in COPD. Ten COPD patients completed a symptom limited incremental cycle exercise. TcPCO2 was measured by a heated electrode on the ear-lobe. Radial artery blood was collected at rest, during unloaded cycling (UL) and every minute during exercise and recovery. Ventilation and gas exchange were measured breath-by-breath. Bland-Altman analysis examined agreement of PCO2 and VD/VT calculated using PaCO2, TcPCO2, end-tidal PCO2 (PETCO2) and estimated PaCO2 by the Jones equation (PaCO2-Jones). Lin’s Concordance Correlation Coefficient (CCC) was assessed. 114 measurements were obtained from the 10 COPD subjects. The bias between TcPCO2 and PaCO2 was 0.86 mmHg with upper and lower limit of agreement ranging −2.28 mmHg to 3.99 mmHg. Correlation between TcPCO2 and PaCO2 during rest and exercise was r2=0.907 (p < 0.001; CCC = 0.941) and VD/VT using TcPCO2 vs. PaCO2 was r2=0.958 (p < 0.0001; CCC = 0.967). Correlation between PaCO2-Jones and PETCO2 vs. PaCO2 were r2=0.755, 0.755, (p < 0.001; CCC = 0.832, 0.718) and for VD/VT calculation (r2=0.793, 0.610; p < 0.0001; CCC = 0.760, 0.448), respectively. The results support the accuracy of TcPCO2 to reflect PaCO2 and calculate VD/VT during rest and exercise, but not in recovery, in COPD patients, enabling improved accuracy of noninvasive assessment of gas exchange inefficiency during incremental exercise testing.

Residual Exertional Dyspnea in Cardiopulmonary Disease.

In cardiopulmonary medicine, residual exertional dyspnea (RED) can be defined by the persistence of limiting breathlessness in a patient who is already under the best available therapy for the underlying heart and/or lung disease. RED is a challenge to the pulmonologist because the patient (and the referring physician) assumes that the "lung doctor" should invariably provide a successful plan to fight the symptom. After presenting a simplified framework to understand the neurobiological underpinnings of dyspnea in cardiorespiratory disease, I discuss the seeds of RED associated with 1) increased metabolic cost of work, 2) increased inspiratory constraints, 3) diaphragm dysfunction, 4) impaired right ventricle preload, 5) increased central and/or peripheral chemosensitivity, 6) increased physiological dead space, 7) increased pulmonary venous and/or high left ventricle filling pressures, 8) impaired chronotropic response to exertion, and 9) increased activation of the cortical-limbic circuits. I finalize by outlining the following two common coexistence of diseases in which these multiple mechanisms interact to produce severe RED: chronic obstructive pulmonary disease-heart failure with reduced ejection fraction and chronic pulmonary fibrosis-emphysema. RED exposes the important limitations of the current reductionist approach focused only on the (over)treatment of the poorly reversible cardiopulmonary disease(s). Conversely, recognizing the existence of RED sets the stage for a more holistic approach toward one of the most devastating symptoms known to man.

Comparing the novel microstream and the traditional mainstream method of end-tidal CO2 monitoring with respect to PaCO2 as gold standard in intubated critically ill children

The objective of this study was to evaluate a novel microstream method by comparison with PaCO2 and the more standard mainstream capnometer in intubated pediatric patients. We hypothesized that the novel microstream method would superior compared to the traditional mainstream method in predicting PaCO2. This was a prospective single-center comparative study. The study was carried out on 174 subjects with a total of 1338 values for each method. Data were collected prospectively from mainstream and microstream capnometer simultaneously and compared with PaCO2 results. Although both mainstream PetCO2 (mainPetCO2) and microstream PetCO2 (microPetCO2) were moderately correlated (r = 0.63 and r = 0.68, respectively) with PaCO2 values, mainPetCO2 was in better agreement with PaCO2 in all subjects (bias ± precision values of 3.8 ± 8.9 and 7.3 ± 8.2 mmHg, respectively). In those with severe pulmonary disease, the mainPetCO2 and microPetCO2 methods were highly correlated with PaCO2 (r = 0.80 and r = 0.81, respectively); however, the biases of both methods increased (14.8 ± 9.1 mmHg and 16.2 ± 9.0 mmHg, respectively). In cases with increased physiologic dead space ventilation, the agreement levels of mainPetCO2 and microPetCO2 methods became distorted (bias ± precision values of 20.9 ± 11.2 and 25.0 ± 11.8 mm Hg, respectively) even though mainPetCO2 and microPetCO2 were highly correlated (r = 0.78 and r = 0.78, respectively). It was found that the novel microstream capnometer method for PetCO2 measurements provided no superiority to the traditional mainstream method. Both capnometer methods may be useful in predicting the trend of PaCO2 due to significant correlations with the gold standard measurement in cases with severe pulmonary disease or increased physiological dead space –despite reduced accuracy.

Respiratory compliances and dead spaces in dogs of various breeds: correlation with corporeal measurements – preliminary results

Introduction: The aim of this study was to measure respiratory system (Crs), chest wall (Ccw) and lung (CL) compliances as well as anatomic (VDanat) and physiologic dead spaces (VDPhys) in dogs of different breeds, and to correlate them with body weight (BW), thoracic circumference (TC), thoracic height (TH), vertebral column length (VC) and skull index (SKI).

Observational study of the use of recombinant tissue-type plasminogen activator in COVID-19 shows a decrease in physiological dead space.

#COVID19-induced ARDS is partly explained by the presence of microthrombi, motivating the use of thrombolytics. This study shows that thrombolytics decrease dead space ventilation in COVID-19 ARDS patients. https://bit.ly/2GdM44a

RARE GASTROBRONCHIAL FISTULA MISTAKEN FOR ASPIRATION PNEUMONIA IN A PATIENT WITH ESOPHAGEAL CANCER: A CASE REPORT

SESSION TITLE: Medical Student/Resident Disorders of the Mediastinum Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Aspiration pneumonia in the setting of known esophageal cancer typically raises suspicion for dysphagia as the primary cause. Here, however, we present a rare case caused by a gastrobronchial fistula (GBF). This study was written according to the CARE case report guidelines [1]. CASE PRESENTATION: A 64 year old Caucasian female with stage IV esophageal cancer presented with acute nausea, vomiting and dyspnea. She had completed radiation and chemotherapy and underwent esophagogastrectomy with gastric pull through eight months prior. She presented with pulmonary sepsis and was treated with antibiotics. She then became acutely hypoxic and hypercapnic and required emergent intubation. An ETT cuff leak persisted despite radiographic confirmation of placement and appropriate cuff inflation. An urgent bronchoscopy showed bilious, projectile material in the RLL. An upper GI series – challenging given the high volume of gastric reflux – opacified the right mainstem bronchus below the carina. Concurrent bronchoscopy/endoscopy visualized a 1 cm gastric fistula at the surgical anastomosis without evidence of ulceration, infection or recurrent neoplasm, communicating with the posterior bronchus intermedius. Successful fistula closure was achieved with endoscopic OverStitch (TM). DISCUSSION: GBFs are rare, and can occur in the setting of infection, neoplasm, trauma or ulcers [2]. One clue is a persistent ETT cuff leak and a high volume of gastric contents refluxing into the ventilatory circuit. The persistence of hypercapnia despite high minute ventilation (presumably from increased physiologic dead space) should also raise suspicion for GBF [2]. GBFs are rarer than esophagobronchial fistulas. In this case, the proximity of the bronchial tree to the thoracic gastric pull through likely contributed to the GBF. A novel feature of this case was the treatment, achieved via an endoscopic OverStitch. Whereas typical treatment might involve the placement of stents on both sides of an enteropulmonic fistula, the OverStitch technique is able to create a tighter, full thickness closure without the complications of in-dwelling stents [3]. CONCLUSIONS: In patients with refractory aspiration pneumonia and an esophagogastric surgical history, consider GBF as a possible cause. Initial testing is an upper GI series followed by dual bronchoscopy and endoscopy for diagnosis and fistulotomy. Reference #1: Riley DS, Barber MS, Kienle GS, AronsonJK, et al. CARE guidelines for case reports: explanation and elaboration document. JClinEpi 2017 Sep;89:218-235. doi: 10.1016/jclinepi.2017.04.026 Reference #2: Greenberg S, Kanth N, Kanth A. A woman with cough: gastrobronchial fistula as a delayed complication of bariatric surgery. Case report and literature review. Am J Emerg Med. 2015;33(4):597.e1-597.e5972. doi:10.1016/j.ajem.2013.11.022 Reference #3: Chon SH, Toex U, Plum PS, et al. Efficacy and feasibility of OverStitch suturing of leaks in the upper gastrointestinal tract [published online ahead of print, 2019 Oct 7]. Surg Endosc. 2019;10.1007/s00464-019-07152-8. doi:10.1007/s00464-019-07152-8 DISCLOSURES: No relevant relationships by Alan Gandler, source=Web Response No relevant relationships by Eric Gold, source=Web Response No relevant relationships by Prarthna Kulandaisamy, source=Web Response

Physiological mechanism and spatial distribution of increased alveolar dead-space in early ARDS: An experimental study.

We aimed to investigate the physiological mechanism and spatial distribution of increased physiological dead-space, an early marker of ARDS mortality, in the initial stages of ARDS. We hypothesized that: increased dead-space results from the spatial redistribution of pulmonary perfusion, not ventilation; such redistribution is not related to thromboembolism (ie, areas with perfusion=0 and infinite ventilation-perfusion ratio, ), but rather to moderate shifts of perfusion increasing in non-dependent regions. Five healthy anesthetized sheep received protective ventilation for 20hours, while endotoxin was continuously infused. Maps of voxel-level lung ventilation, perfusion, , CO2 partial pressures, and alveolar dead-space fraction were estimated from positron emission tomography at baseline and 20hours. Alveolar dead-space fraction increased during the 20hours (+0.05, P=.031), mainly in non-dependent regions (+0.03, P=.031). This was mediated by perfusion redistribution away from non-dependent regions (-5.9%, P=.031), while the spatial distribution of ventilation did not change, resulting in increased in non-dependent regions. The increased alveolar dead-space derived mostly from areas with intermediate (0.5≤ ≤10), not areas of nearly "complete" dead-space ( >10). In this early ARDS model, increases in alveolar dead-space occur within 20hours due to the regional redistribution of perfusion and not ventilation. This moderate redistribution suggests changes in the interplay between active and passive perfusion redistribution mechanisms (including hypoxic vasoconstriction and gravitational effects), not the appearance of thromboembolism. Hence, the association between mortality and increased dead-space possibly arises from the former, reflecting gas-exchange inefficiency due to perfusion heterogeneity. Such heterogeneity results from the injury and exhaustion of compensatory mechanisms for perfusion redistribution.

Early experience with critically ill patients with COVID-19 in Montreal.

PurposeMontreal has been the epicentre of the coronavirus disease (COVID-19) pandemic in Canada. Given the regional disparities in incidence and mortality in the general population, we aimed to describe local characteristics, treatments, and outcomes of critically ill COVID-19 patients in Montreal.MethodsA single-centre retrospective cohort of consecutive adult patients admitted to the intensive care unit (ICU) of Hôpital du Sacré-Coeur de Montréal with confirmed COVID-19 were included.ResultsBetween 20 March and 13 May 2020, 75 patients were admitted, with a median [interquartile range (IQR)] age of 62 [53–72] yr and high rates of obesity (47%), hypertension (67%), and diabetes (37%). Healthcare-related infections were responsible for 35% of cases. The median [IQR] day 1 sequential organ failure assessment score was 6 [3–7]. Invasive mechanical ventilation (IMV) was used in 57% of patients for a median [IQR] of 11 [5–22] days. Patients receiving IMV were characterized by a moderately decreased median [IQR] partial pressure of oxygen:fraction of inspired oxygen (day 1 PaO2:FiO2 = 177 [138–276]; day 10 = 173 [147–227]) and compliance (day 1 = 48 [38–58] mL/cmH2O; day 10 = 34 [28–42] mL/cmH2O) and very elevated estimated dead space fraction (day 1 = 0.60 [0.53–0.67]; day 10 = 0.72 [0.69–0.79]). Overall hospital mortality was 25%, and 21% in the IMV patients. Mortality was 82% in patients ≥ 80 yr old.ConclusionsCharacteristics and outcomes of critically ill patients with COVID-19 in Montreal were similar to those reported in the existing literature. We found an increased physiologic dead space, supporting the hypothesis that pulmonary vascular injury may be central to COVID-19-induced lung damage.

In Response.

We thank Dr A. K. Jha1 for his valuable comments regarding our article.2 Although there is a correlation between the relative perfusion to the operative lung as assessed by lung scans and the partial pressure of oxygen in arterial blood (Pao2), it is unclear whether this variable is clinically relevant for patients undergoing thoracic surgery.3 Because not all the patients enrolled in our trial underwent lung perfusion scans, we did not perform a between-group comparison. We also did not measure Pao2 levels by arterial blood gas analysis during 2-lung ventilation (TLV). Because the Pao2 level during 1-lung ventilation (OLV) strongly and positively correlates with Pao2 during TLV, we were able to predict hypoxemia during OLV for patients in both groups that presented with an average room air saturation of 93% before general anesthesia. Nonetheless, we acknowledge that the TLV parameters and preoperative perfusion scans may give more insight on the impact of OLV, peak inspiratory pressure (PIP) and Pao2/fractional inspiration of oxygen (Fio2) (P/F) ratio. Hypoxic pulmonary vasoconstriction (HPV) during OLV mitigates the shunt fraction. HPV is blunted by sevoflurane and suppressed by the pathologic effects of chronic obstructive pulmonary disease (COPD). Although we did measure sevoflurane concentrations, we administered balanced anesthesia that included a remifentanil infusion. Thus, the actual concentration of sevoflurane was probably less than 1 minimum alveolar concentration (MAC), a concentration thought to have limited impact on HPV.4 Also, the treatment of OLV-induced increase in pulmonary hypertension may have been beneficial, as Dr A. K. Jha1 commented in the letter. Unfortunately, as we mentioned in the limitation section, we can only speculate there was an OLV-induced rise in pulmonary artery pressure because it was not possible to obtain accurate measurements of pulmonary arterial pressure in our clinical practice. We agree with the view that iloprost-induced pulmonary arteriolar vasodilation in the ventilated lung resulted in blood diversion from nonventilated lung to the ventilated lung with physiological dead space reduction and P/F ratio augmentation. Indeed, as our study results indicate, inhaled iloprost improves oxygenation and dead space ventilation during OLV in COPD patients with poor lung oxygenation. Considering that atelectasis in the operated lung persists in the postoperative period,5 it can be deduced that the difference in P/F ratio in the postanesthetic care unit in both groups may be due to the residual intrapulmonary shunt fraction and the residual effects of iloprost inhalation, which ameliorates the ventilation/perfusion matching. In this regard, we speculate that the beneficial effects of iloprost during OLV may persist even after TLV or spontaneous ventilation is restored, but this needs to be clarified. We think that the comments provided by Dr A. K. Jha1 are valuable and should be considered when planning further studies. Namo Kim, MD, PhDDepartment of Anesthesiology and Pain MedicineAnesthesia and Pain Research InstituteYonsei University College of MedicineSeoul, Republic of Korea Su Hyun Lee, MDDepartment of Anesthesiology and Pain MedicineYonsei Sarang HospitalSeoul, Republic of Korea Young Jun Oh, MD, PhDDepartment of Anesthesiology and Pain MedicineAnesthesia and Pain Research InstituteYonsei University College of MedicineSeoul, Republic of Korea[email protected]

Increased physiological dead space in mechanically ventilated COVID-19 patients recovering from severe acute respiratory distress syndrome: a case report

BackgroundAn ongoing outbreak of coronavirus disease 2019 (COVID-19) is spreading globally. Recently, several articles have mentioned that the early acute respiratory distress syndrome (ARDS) caused by COVID-19 significantly differ from those of ARDS due to other causes. Actually, we newly observed that some mechanically ventilated COVID-19 patients recovering from severe ARDS (more than 14 days after invasive ventilation) often experienced evidently gradual increases in CO2 retention and minute ventilation. However, the underlying mechanics remain unclear.Case presentationTo explain these pathophysiological features and discuss the ventilatory strategy during the late phase of severe ARDS in COVID-19 patients, we first used a metabolic module on a General Electric R860 ventilator (Engstrom Carestation; GE Healthcare, USA) to monitor parameters related to gas metabolism, lung mechanics and physiological dead space in two COVID-19 patients. We found that remarkably decreased ventilatory efficiency (e.g., the ratio of dead space to tidal volume 70–80%, arterial to end-tidal CO2 difference 18–23 mmHg and ventilatory ratio 3–4) and hypermetabolism (oxygen consumption 300–400 ml/min, CO2 elimination 200–300 ml/min) may explain why these patients experienced more severe respiratory distress and CO2 retention in the late phase of ARDS caused by COVID-19.ConclusionDuring the recovery period of ARDS among mechanically-ventilated COVID-19 patients, attention should be paid to the monitoring of physiological dead space and metabolism. Tidal volume (8–9 ml/kg) could be increased appropriately under the limited plateau pressure; however, barotrauma should still be kept in mind.

Reversible platypnea-orthodeoxia in COVID-19 acute respiratory distress syndrome survivors

Platypnea-orthodeoxia syndrome (POS) is a rare clinical syndrome characterized by orthostatic oxygen desaturation and positional dyspnea from supine to an upright position. We observed POS in 5 of 20 cases of severe 2019 novel coronavirus (COVID-19) pneumonia, which demonstrated persistently elevated shunt fraction even after liberation from mechanical ventilation. POS was first observed during physiotherapy sessions; median oxygen desaturation was 8 % (range: 8–12 %). Affected individuals were older (median 64 vs 53 years old, p = 0.05) and had lower body mass index (median 24.7 vs 27.6 kg/m2, p = 0.03) compared to those without POS. While POS caused alarm and reduced tolerance to therapy, this phenomenon resolved over a median of 17 days with improvement of parenchymal disease. The mechanisms of POS are likely due to gravitational redistribution of pulmonary blood flow resulting in increased basal physiological shunting and upper zone dead space ventilation due to the predominantly basal distribution of consolidative change and reported vasculoplegia and microthrombi in severe COVID-19 disease.

Reduction in minute alveolar ventilation causes hypercapnia in ventilated neonates with respiratory distress.

Hypercapnia occurs in ventilated infants even if tidal volume (VT) and minute ventilation (VE) are maintained. We hypothesised that increased physiological dead space (Vd,phys) caused decreased minute alveolar ventilation (VA; alveolar ventilation (VA) × respiratory rate) in well-ventilated infants with hypercapnia. We investigated the relationship between dead space and partial pressure of carbon dioxide (PaCO2) and assessed VA. Intubated infants (n = 33; mean birth weight, 2257 ± 641 g; mean gestational age, 35.0 ± 3.3 weeks) were enrolled. We performed volumetric capnography (Vcap), and calculated Vd,phys and VA when arterial blood sampling was necessary. PaCO2 was positively correlated with alveolar dead space (Vd,alv) (r = 0.54, p < 0.001) and Vd,phys (r = 0.48, p < 0.001), but not Fowler dead space (r = 0.14, p = 0.12). Normocapnia (82 measurements; 35 mmHg ≤ PaCO2 < 45 mmHg) and hypercapnia groups (57 measurements; 45 mmHg ≤ PaCO2) were classified. The hypercapnia group had higher Vd,phys (median 0.57 (IQR, 0.44–0.67)) than the normocapnia group (median Vd,phys/VT = 0.46 (IQR, 0.37–0.58)], with no difference in VT. The hypercapnia group had lower VA (123 (IQR, 87–166) ml/kg/min) than the normocapnia group (151 (IQR, 115–180) ml/kg/min), with no difference in VE.Conclusion: Reduction of VA in well-ventilated neonates induces hypercapnia, caused by an increase in Vd,phys.What is Known: • Volumetric capnography based on ventilator graphics and capnograms is a useful tool in determining physiological dead space of ventilated infants and investigating the cause of hypercapnia.What is New:• This study adds evidence that reduction in minute alveolar ventilation causes hypercapnia in ventilated neonates.

Severe, transient pulmonary ventilation-perfusion mismatch in the lung after porcine high velocity projectile behind armor blunt trauma

Background Behind armor blunt trauma (BABT) is a non-penetrating injury caused by the rapid deformation of body armor, by a projectile, which may in extreme circumstances cause death. Although there is not a high incidence of high energy BABT, the understanding of the mechanisms is still low, in relation to what is needed for safety threshold levels. BABT is also useful as a model for blunt thoracic trauma, with a compressive speed between traffic accidents and blast caused by explosives. High velocity projectile BABT causes severe hypoxia. The mechanisms are not fully known. We investigated the acute pulmonary consequences in the individual lungs, and the effects of alveolar recruitment. Methods 12 swine (mean weight 62.5 kg) were randomized to groups BABT by 7.62 × 51 mm NATO-type bullets (mean velocity 803 m/s) to a military grade ceramic plate armor (n = 7) or control (n = 5). Modified double lumen tracheal tubes provided respiratory dynamics in the lungs separately/intermittently for two hours, with alveolar recruitment after one hour. Results Venous admixture increased 5 min after BABT (p < .05) and correlated with increased cardiac output. Static compliance decreased 5 minutes after BABT (p < .05) and further by recruitment (p < .005). Physiological dead space decreased 5 minutes after BABT (p < .01) and further by recruitment (p < .01), while not in the contralateral lung. V′A/Q′ decreased 5 minutes after BABT (p < .05), also shown in phase III volumetric capnography (p < .05). Most effects regressed after one hour. Conclusions High velocity projectile BABT caused hypoxia by a severe and transient decrease in V′A/Q′ to <1 and increased venous admixture in the exposed lung. Alveolar recruitment was hemodynamically and respiratory tolerable and increased V′A/Q′. Body armor development should aim at ameliorating severe pulmonary consequences from high projectile velocities which also needs to include further understanding of how primary and secondary effects are distributed between the lungs.

Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study

RationaleCOVID-19 ARDS could differ from typical forms of the syndrome.ObjectivePulmonary microvascular injury and thrombosis are increasingly reported as constitutive features of COVID-19 respiratory failure. Our aim was to study pulmonary mechanics and gas exchanges in COVID-2019 ARDS patients studied early after initiating protective invasive mechanical ventilation, seeking after corresponding pathophysiological and biological characteristics.MethodsBetween March 22 and March 30, 2020 respiratory mechanics, gas exchanges, circulating endothelial cells (CEC) as markers of endothelial damage, and D-dimers were studied in 22 moderate-to-severe COVID-19 ARDS patients, 1 [1–4] day after intubation (median [IQR]).Measurements and main resultsThirteen moderate and 9 severe COVID-19 ARDS patients were studied after initiation of high PEEP protective mechanical ventilation. We observed moderately decreased respiratory system compliance: 39.5 [33.1–44.7] mL/cmH2O and end-expiratory lung volume: 2100 [1721–2434] mL. Gas exchanges were characterized by hypercapnia 55 [44–62] mmHg, high physiological dead-space (VD/VT): 75 [69–85.5] % and ventilatory ratio (VR): 2.9 [2.2–3.4]. VD/VT and VR were significantly correlated: r2 = 0.24, p = 0.014. No pulmonary embolism was suspected at the time of measurements. CECs and D-dimers were elevated as compared to normal values: 24 [12–46] cells per mL and 1483 [999–2217] ng/mL, respectively.ConclusionsWe observed early in the course of COVID-19 ARDS high VD/VT in association with biological markers of endothelial damage and thrombosis. High VD/VT can be explained by high PEEP settings and added instrumental dead space, with a possible associated role of COVID-19-triggered pulmonary microvascular endothelial damage and microthrombotic process.

Combining Dynamic Hyperinflation with Dead Space Volume during Maximal Exercise in Patients with Chronic Obstructive Pulmonary Disease.

Physiological dead space volume (VD) and dynamic hyperinflation (DH) are two different types of abnormal pulmonary physiology. Although they both involve lung volume, their combination has never been advocated, and thus their effect and implication are unclear. This study aimed (1) to combine VD and DH, and (2) investigate their relationship and clinical significance during exercise, as well as (3) identify a noninvasive variable to represent the VD fraction of tidal volume (VD/VT). Forty-six male subjects with chronic obstructive pulmonary disease (COPD) and 34 healthy male subjects matched for age and height were enrolled. Demographic data, lung function, and maximal exercise were investigated. End-expiratory lung volume (EELV) was measured for the control group and estimated for the study group using the formulae reported in our previous study. The VD/VT ratio was measured for the study group, and reference values of VD/VT were used for the control group. In the COPD group, the DHpeak/total lung capacity (TLC, DHpeak%) was 7% and the EELVpeak% was 70%. After adding the VDpeak% (8%), the VDDHpeak% was 15% and the VDEELVpeak% was 78%. Both were higher than those of the healthy controls. In the COPD group, the VDDHpeak% and VDEELVpeak% were more correlated with dyspnea score and exercise capacity than that of the DHpeak% and EELV%, and had a similar strength of correlation with minute ventilation. The VTpeak/TLC (VTpeak%), an inverse marker of DH, was inversely correlated with VD/VT (R2 ≈ 0.50). Therefore, we recommend that VD should be added to DH and EELV, as they are physiologically meaningful and VTpeak% represents not only DH but also dead space ventilation. To obtain VD, the VD/VT must be measured. Because obtaining VD/VT requires invasive arterial blood gases, further studies on noninvasive predicting VD/VT is warranted.

Standardizing the cerebrovascular response to hypercapnia - increasing the flow of data!

Standardizing the cerebrovascular response to hypercapnia - increasing the flow of data!

Management of hypercapnia in critically ill mechanically ventilated patients-A narrative review of literature.

The use of lower tidal volume ventilation was shown to improve survival in mechanically ventilated patients with acute lung injury. In some patients this strategy may cause hypercapnic acidosis. A significant body of recent clinical data suggest that hypercapnic acidosis is associated with adverse clinical outcomes including increased hospital mortality. We aimed to review the available treatment options that may be used to manage acute hypercapnic acidosis that may be seen with low tidal volume ventilation. The databases of MEDLINE and EMBASE were searched. Studies including animals or tissues were excluded. We also searched bibliographic references of relevant studies, irrespective of study design with the intention of finding relevant studies to be included in this review. The possible options to treat hypercapnia included optimising the use of low tidal volume mechanical ventilation to enhance carbon dioxide elimination. These include techniques to reduce dead space ventilation, and physiological dead space, use of buffers, airway pressure release ventilation and prone positon ventilation. In patients where hypercapnic acidosis could not be managed with lung protective mechanical ventilation, extracorporeal techniques may be used. Newer, minimally invasive low volume venovenous extracorporeal devices are currently being investigated for managing hypercapnia associated with low and ultra-low volume mechanical ventilation.

Prone Positioning for Acute Respiratory Distress Syndrome in Adults.

Prone Positioning for Acute Respiratory Distress Syndrome in Adults.

ОПРЕДЕЛЕНИЕ ОБЪЁМА ДЫХАТЕЛЬНЫХ МЁРТВЫХ ПРОСТРАНСТВ МЕТОДОМ КАПНОВОЛЮМЕТРИИ

The article provides information on the lung dead space – a part of the respiratory volume that does not participate in gas exchange. The anatomical and alveolar dead spaces jointly together form the physiological dead space. The article describes methods for determining the volume of dead spaces using the capnovolumetry. The volume of physiological dead space is calculated using the C. Bohr equation. The volume of anatomical dead space can be determined using the equal area method proposed by W.S. Fowler. The volume of the alveolar dead space is the difference of volumes of the physiological and anatomical dead spaces. In pathology, the volume of the alveolar space and, consequently, physiological dead space can increase significantly. Determination of the volume of dead space is the significant criterion for diagnostic and predicting the outcome of a number of diseases. Keywords: Physiological dead space , anatomical dead space , alveolar dead space , capnovolumetry, volumetric capnography.

Dyspnea Postpulmonary Embolism From Physiological Dead Space Proportion and Stroke Volume Defects During Exercise

Many patients with pulmonary embolism (PE) report dyspnea on exertion following long-term treatment. Increased physiological dead space proportion (VD/VT) and decreased cardiac stroke volume reserve may distinguish persistent effects of PE itself from symptoms reflecting comorbid conditions or deconditioning. This retrospective study analyzed a consecutive series of incremental symptom-limited cardiopulmonary exercise tests that had been ordered to evaluate persistent dyspnea on exertion following long-term treatment for acute PE. Physiological VD/VT was determined at anaerobic threshold from exhaled CO2 and transcutaneous Pco2 (validated against Paco2 measurements). Cardiac stroke volume reserve was estimated at rest and at anaerobic threshold by using oxygen consumption/pulse and previously validated estimates of the arteriovenous oxygen content difference. Cardiopulmonary exercise tests were performed on 40 patients with post-PE dyspnea. In 65.0%(95%CI, 50.2-79.8), VD/VT at anaerobic threshold was abnormally elevated, stroke volume reserve was decreased, or both defects occurred. VD/VT at anaerobic threshold was abnormally elevated (≥ 0.27) in 35.0%(95%CI, 20.2-49.8). VD/VT at anaerobic threshold significantly correlated with the extent of unmatched perfusion defects on subsequent ventilation-perfusion scans (P= .0085). In 55.0%(95%CI, 39.6-70.4), stroke volume reserve at anaerobic threshold was abnormally decreased (≤ 128%of the resting value). Both defects were present in 25.0%(95%CI, 11.6-38.4). Increased VD/VT at anaerobic threshold and decreased stroke volume reserve during exercise are common among patients with dyspnea on exertion after long-term treatment of PE. The defects can be disclosed noninvasively by using cardiopulmonary exercise testing.