Bedside estimates of dead space using end-tidal CO2 are independently associated with mortality in ARDS

Lecompte-Osorio, Paola; Pearson, Steven D; Pieroni, Cole H.; Stutz, Matthew R; Pohlman, Anne S.; Lin, Julie; Hall, Jesse B.; Htwe, Yu Maw; Belvitch, Patrick; Dudek, Steven M.; Wolfe, K.S.; Patel, Bhakti; Kress, John P.

doi:10.1186/s13054-021-03751-x

Cited by 21 publications

(13 citation statements)

References 23 publications

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“…Five studies assessed both V D /V T and VR (27,(29)(30)(31)33). Other indices assessed were end-tidal to arterial carbon dioxide ratio (29,39), corrected minute ventilation (30), and arterial to end-tidal carbon dioxide gradient (28). The median mortality rate was 36.4% (IQR 28.6%-44.0%), and median Pao 2 /Fio 2 in the V D /V T and VR cohorts was 152 (IQR 134-170) and 138 (IQR 130-155), respectively.…”

Section: Resultsmentioning

confidence: 99%

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Dead-Space Ventilation Indices and Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis*

Jayasimhan¹,

Chieng²,

Kolbe

et al. 2023

Critical Care Medicine

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OBJECTIVES: Acute respiratory distress syndrome (ARDS) is associated with high ventilation-perfusion heterogeneity and dead-space ventilation. However, whether the degree of dead-space ventilation is associated with outcomes is uncertain. In this systematic review and meta-analysis, we evaluated the ability of dead-space ventilation measures to predict mortality in patients with ARDS. DATA SOURCES: MEDLINE, CENTRAL, and Google Scholar from inception to November 2022. STUDY SELECTION: Studies including adults with ARDS reporting a dead-space ventilation index and mortality. DATA EXTRACTION: Two reviewers independently identified eligible studies and extracted data. We calculated pooled effect estimates using a random effects model for both adjusted and unadjusted results. The quality and strength of evidence were assessed using the Quality in Prognostic Studies and Grading of Recommendations, Assessment, Development, and Evaluation, respectively. DATA SYNTHESIS: We included 28 studies in our review, 21 of which were included in our meta-analysis. All studies had a low risk of bias. A high pulmonary dead-space fraction was associated with increased mortality (odds ratio [OR], 3.52; 95% CI, 2.22–5.58; p < 0.001; I 2 = 84%). After adjusting for other confounding variables, every 0.05 increase in pulmonary-dead space fraction was associated with an increased odds of death (OR, 1.23; 95% CI, 1.13–1.34; p < 0.001; I 2 = 57%). A high ventilatory ratio was also associated with increased mortality (OR, 1.55; 95% CI, 1.33–1.80; p < 0.001; I 2 = 48%). This association was independent of common confounding variables (OR, 1.33; 95% CI, 1.12–1.58; p = 0.001; I 2 = 66%). CONCLUSIONS: Dead-space ventilation indices were independently associated with mortality in adults with ARDS. These indices could be incorporated into clinical trials and used to identify patients who could benefit from early institution of adjunctive therapies. The cut-offs identified in this study should be prospectively validated.

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Section: Resultsmentioning

confidence: 99%

“…Some studies had more than one cohort of patients for derivation and subsequent validation. We included 29 studies comprising 33 cohorts in our systematic review (5, 9, 10, 18–43) and 16 studies comprising 21 cohorts in our meta-analysis ( Fig. 1 ).…”

Section: Resultsmentioning

confidence: 99%

Dead-Space Ventilation Indices and Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis*

Jayasimhan¹,

Chieng²,

Kolbe

et al. 2023

Critical Care Medicine

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“…Mechanical ventilation and other respiratory support strategies (non-invasive ventilation and high-flow oxygen therapy) do not affect the V/Q ratio in intact ventilation and perfusion pathology, while the positive effects of prone position on oxygenation can be explained by the gravitational redistribution of blood flow to intact areas with high V/Q ratio and a cumulative V/Q optimization in general. At the same time the increase in alveolar dead space is independently associated with mortality in ARDS [ 32 ]. This pathophysiological theory supports the early use of pulmonary vasodilators, such as iNO ( Figure 1 ) [ 8 , 9 ].…”

Section: Historical Benefits Of No: Ino As Selective Pulmonary Vasodi...mentioning

confidence: 99%

Therapeutic Effects of Inhaled Nitric Oxide Therapy in COVID-19 Patients

Каменщиков

Carroll

2022

Biomedicines

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The global COVID-19 pandemic has become the largest public health challenge of recent years. The incidence of COVID-19-related acute hypoxemic respiratory failure (AHRF) occurs in up to 15% of hospitalized patients. Antiviral drugs currently available to clinicians have little to no effect on mortality, length of in-hospital stay, the need for mechanical ventilation, or long-term effects. Inhaled nitric oxide (iNO) administration is a promising new non-standard approach to directly treat viral burden while enhancing oxygenation. Along with its putative antiviral affect in COVID-19 patients, iNO can reduce inflammatory cell-mediated lung injury by inhibiting neutrophil activation, lowering pulmonary vascular resistance and decreasing edema in the alveolar spaces, collectively enhancing ventilation/perfusion matching. This narrative review article presents recent literature on the iNO therapy use for COVID-19 patients. The authors suggest that early administration of the iNO therapy may be a safe and promising approach for the treatment of COVID-19 patients. The authors also discuss unconventional approaches to treatment, continuous versus intermittent high-dose iNO therapy, timing of initiation of therapy (early versus late), and novel delivery systems. Future laboratory and clinical research is required to define the role of iNO as an adjunct therapy against bacterial, viral, and fungal infections.

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“…Surprisingly, COVID-19 patients may achieve a high P aCO 2 -P ETCO 2 gap, sometimes exceeding the predicted cut-off values of mortality in non-COVID-19 acute respiratory distress syndrome (ARDS) patients (i.e. 10-15 mmHg) [4]. Observing the data presented by VIOLA et al [5] in type L COVID-19 pneumonia patients, we have found a median P aCO 2 -P ETCO 2 gap for supine position of 20.6 mmHg and 14.9 mmHg for prone position.…”

mentioning

confidence: 92%

“…3 Erebouni medical center, Dept of Anesthesiology, Yerevan, Armenia. 4 National Center for Infection Diseases (Ministry of Health, Republic of Armenia), Yerevan, Armenia. 5 Ministry of Health, Republic of Armenia, Yerevan, Armenia.…”

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confidence: 99%

Ventilation/perfusion mismatch is not the sole reason for hypoxaemia in early stage COVID-19 patients

Harutyunyan¹,

Harutyunyan

et al. 2022

Eur Respir Rev

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It was a pleasure reading the work of GATTINONI et al. [1] dedicated to the pathophysiological mechanisms of hypoxaemia observed in coronavirus disease 2019 patients. The authors recommend treating the hypoxaemia observed in the early stages of COVID-19 based on ventilation/perfusion (Vʹ A /Qʹ) mismatch.According to the laws of physics, increasing fractional concentration of oxygen in inspired gas (F IO 2 ) can increase arterial blood oxygen saturation (S aO 2 ) in case of Vʹ A /Qʹ <1. Also, it should be recognised that oxygen, as an important homotropic allosteric effector, favours the stabilisation of the quaternary R (relaxed) state of haemoglobin (Hb) allowing for an increase in S aO 2 by a positive feedback mechanism (binding of oxygen to Hb facilitates binding of new oxygen molecules). These biochemical processes may improve the S aO 2 in patients with decreased Hb-O 2 affinity in alveolar capillaries without any Vʹ A /Qʹ mismatch. Therefore, in cases of "happy" hypoxia or silent hypoxaemia, an exaggerated increase in S aO 2 with minimal hyperoxia may take place due to the allosteric effects of oxygen rather than Vʹ A /Qʹ maldistribution. Also, a high level of oxygen dependency is commonly seen in all stages of COVID-19 with frequent use of high F IO 2 without of development of atelectasis in the hypoventilated areas of the lungs, which also can't be explained by the Vʹ A /Qʹ mismatch.A discussion of CO 2 gas exchange mechanisms will further clarify the course of events resulting in hypoxaemia in COVID-19 patients. The remarkable increase in tidal volume in a patient with COVID-19 can be understood from the biochemical point of view: elimination of CO 2 , which is a strong heterotropic allosteric effector, will result in stabilisation of Hb's R state and assists its complete oxygenation.As we know, during hypoventilation, the gases are balanced in the alveolar-capillary space. Hence, a decreased Vʹ A /Qʹ ratio will result in a higher alveolar (P ACO 2 ) and arterial carbon dioxide tension (P aCO 2 ), but won't change the P aCO 2 and end-tidal carbon dioxide tension (P ETCO 2 ) gap [2]. Also, due to the low resistance to diffusion of CO 2 , P aCO 2 -P ETCO 2 gap is maintained unchanged in cases when patients have oxygen diffusion limitations [3]. Surprisingly, COVID-19 patients may achieve a high P aCO 2 -P ETCO 2 gap, sometimes exceeding the predicted cut-off values of mortality in non-COVID-19 acute respiratory distress syndrome (ARDS) patients (i.e. 10-15 mmHg) [4]. Observing the data presented by VIOLA et al. [5] in type L COVID-19 pneumonia patients, we have found a median P aCO 2 -P ETCO 2 gap for supine position of 20.6 mmHg and 14.9 mmHg for prone position. BUSANA et al. [6] reported a P aCO 2 -P ETCO 2 gap of 15 mmHg in COVID-19 patients who need a high F IO 2 to maintain S aO 2 . In critically ill COVID-19 patients, as presented by CHEN et al. [7], the P aCO 2 -P ETCO 2 gap is reached at very high levels of 33 mmHg (18-40 mmHg). So, considering excessively high levels of the P aCO 2 -P ETCO 2 g...

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Bedside estimates of dead space using end-tidal CO2 are independently associated with mortality in ARDS

Cited by 21 publications

References 23 publications

Dead-Space Ventilation Indices and Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis*

Dead-Space Ventilation Indices and Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis*

Therapeutic Effects of Inhaled Nitric Oxide Therapy in COVID-19 Patients

Ventilation/perfusion mismatch is not the sole reason for hypoxaemia in early stage COVID-19 patients

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