Tissue Hypoxia: Implications for the Respiratory Clinician

MacIntyre, Neil R.

doi:10.4187/respcare.03357

Cited by 89 publications

(64 citation statements)

References 58 publications

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“…Acute respiratory distress syndrome (ARDS) is a syndrome characterized by impaired gas exchange resulting in low oxygen tensions in the blood (i.e., hypoxemia) and tissues (i.e., hypoxia) [1]. Tissue hypoxia is harmful, leading to cell death, organ failure, and increased mortality in the critically ill [2]. While oxygen therapy can reverse tissue hypoxia, little evidence exists regarding the optimal use of oxygen in patients with ARDS.…”

Section: Introductionmentioning

confidence: 99%

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome: insights from the LUNG SAFE study

et al. 2020

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Background: Concerns exist regarding the prevalence and impact of unnecessary oxygen use in patients with acute respiratory distress syndrome (ARDS). We examined this issue in patients with ARDS enrolled in the Large observational study to UNderstand the Global impact of Severe Acute respiratory FailurE (LUNG SAFE) study. Methods:In this secondary analysis of the LUNG SAFE study, we wished to determine the prevalence and the outcomes associated with hyperoxemia on day 1, sustained hyperoxemia, and excessive oxygen use in patients with early ARDS. Patients who fulfilled criteria of ARDS on day 1 and day 2 of acute hypoxemic respiratory failure were categorized based on the presence of hyperoxemia (PaO 2 > 100 mmHg) on day 1, sustained (i.e., present on day 1 and day 2) hyperoxemia, or excessive oxygen use (FIO 2 ≥ 0.60 during hyperoxemia). Results: Of 2005 patients that met the inclusion criteria, 131 (6.5%) were hypoxemic (PaO 2 < 55 mmHg), 607 (30%) had hyperoxemia on day 1, and 250 (12%) had sustained hyperoxemia. Excess FIO 2 use occurred in 400 (66%) out of 607 patients with hyperoxemia. Excess FIO 2 use decreased from day 1 to day 2 of ARDS, with most hyperoxemic patients on day 2 receiving relatively low FIO 2 . Multivariate analyses found no independent relationship between day 1 hyperoxemia, sustained hyperoxemia, or excess FIO 2 use and adverse clinical outcomes. Mortality was 42% in patients with excess FIO 2 use, compared to 39% in a propensity-matched sample of normoxemic (PaO 2 55-100 mmHg) patients (P = 0.47).Conclusions: Hyperoxemia and excess oxygen use are both prevalent in early ARDS but are most often non-sustained. No relationship was found between hyperoxemia or excessive oxygen use and patient outcome in this cohort. Trial registration: LUNG-SAFE is registered with ClinicalTrials.gov, NCT02010073

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Section: Introductionmentioning

confidence: 99%

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome: insights from the LUNG SAFE study

et al. 2020

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“…Deleterious effects of hypoxia through the multiple downstream effects of poor tissue oxygenation include increased cardiac strain, pulmonary hypertension and salt and water imbalance mediated through the impact of cardiac and circulatory insufficiency (Cor Pulmonale). Pathophysiological secondary damage to multiple other organs and tissues including skeletal muscle, brain, kidney and gut are also attributable to impaired O 2 delivery 2 3. In the setting of relative tissue hypoxia and an imbalance between oxygen demand and respiratory capacity, a ‘spiral of decline’ ensues resulting in progressive deconditioning, frailty and both enhanced oxygen demand and increased respiratory loading through premature exercise induced acidosis (figure 2).…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown in COPD that Hb is directly related to oxygen consumption (VO 2 max) even after accounting for disease severity12 and, at a patient level, symptomatic burden and mortality 13 14. Indeed O 2 availability impacts ventilation, pulmonary blood flow and gene expression throughout the body 2. Long-term oxygen therapy (LTOT) is an established therapy that reduces both morbidity15 and mortality16 17 in severely hypoxic patients and, in appropriate populations, supplementing inspired O 2 increases exercise duration 18.…”

Section: Introductionmentioning

confidence: 99%

Anaemia and iron dysregulation: untapped therapeutic targets in chronic lung disease?

et al. 2019

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Hypoxia is common in many chronic lung diseases. Beyond pulmonary considerations, delivery of oxygen (O2) to the tissues and subsequent O2 utilisation is also determined by other factors including red blood cell mass and iron status; consequently, disruption to these mechanisms provides further physiological strains on an already stressed system. O2 availability influences ventilation, regulates pulmonary blood flow and impacts gene expression throughout the body. Deleterious effects of poor tissue oxygenation include decreased exercise tolerance, increased cardiac strain and pulmonary hypertension in addition to pathophysiological involvement of multiple other organs resulting in progressive frailty. Increasing inspired O2 is expensive, disliked by patients and does not normalise tissue oxygenation; thus, other strategies that improve O2 delivery and utilisation may provide novel therapeutic opportunities in patients with lung disease. In this review, we focus on the rationale and possibilities for doing this by increasing haemoglobin availability or improving iron regulation.

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“…Hypoxemia is a dangerous condition because it renders insufficient one of the crucial life-supporting mechanisms, the cellular production of energy. Unfortunately, it results from various, frequent and disabling diseases associated with respiratory and heart failure syndromes [1]. Acute hypoxemia triggers compensatory mechanisms, of which chemoreflex activation is considered the most relevant, because it rises pulmonary ventilation and cardiovascular sympathetic activity, which preserves cardiac output [2,3].…”

Section: Introductionmentioning

confidence: 99%

Instantaneous Time Course of Autonomic-Cardiovascular Response to Short-Term Hypoxia in Healthy Subjects: a Time-Frequency Analysis Approach

Carrasco-Sosa

Guillen-Mandujano

2017

Computing in Cardiology Conference (CinC)

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In ten healthy volunteers, we assessed the effects produced by 2-min 12% O 2 breathing on the instantaneous time course of: arterial oxygen saturation (SaO 2), respiratory frequency (RF), end-tidal CO 2 (ETCO 2), R-R intervals (RR), systolic pressure (SP), diastolic pressure (DP), pulse pressure (PP), maximal amplitude of arterial pressure derivative (dmAP), and, estimated by a time frequency distribution, their low frequency powers (LF RR , LF PP and LF dmAP) and high frequency powers of RR (HF RR) and respiration (HF Res) as well as baroreflex sensitivity (BRS) and respiratory sinus arrhythmia sensitivity (RSAS) by alpha index. Mean SaO 2 of 82±2% provoked consistent response patterns in all variables: with 9-s latency, progressive decrease (p<0.002) until the end of LF dmAP , LF PP , RR, HF RR , RSAS, dmAP, ETCO 2 and BRS (36-s latency), and gradual increase (p<0.004) of RF; with 108-s latency, a sustained decrease (p<0.004) of SP and DP. Hypocapnic hypoxemia provokes: an immediate functional depression shown by gradual reductions of sympathetic and vagal activities that contribute to the progressive fall of RR, RSAS and BRS with unchanged arterial pressure, and, through chemoreflex activation, a progressive increase of RF; and later, via direct vasodilation, a reduction of arterial pressure. 2.2. Protocol Volunteers visited the laboratory twice. The first time, their health status and anthropometric variables were evaluated, and in the second visit the experimental stage

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Tissue Hypoxia: Implications for the Respiratory Clinician

Cited by 89 publications

References 58 publications

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome: insights from the LUNG SAFE study

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome: insights from the LUNG SAFE study

Anaemia and iron dysregulation: untapped therapeutic targets in chronic lung disease?

Instantaneous Time Course of Autonomic-Cardiovascular Response to Short-Term Hypoxia in Healthy Subjects: a Time-Frequency Analysis Approach

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