Cardiovascular effects of hyperoxia during and after cardiac surgery

Man, A.M.E. Spoelstra-de; Smit, Bob; Straaten, Heleen M. Oudemans–van; Smulders, Yvo M.

doi:10.1111/anae.13218

Cited by 58 publications

(49 citation statements)

References 109 publications

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“…There is substantial consensus on the effects that longterm hyperoxia causes in healthy subjects: sympathetic activity decrease, as evaluated by muscular sympathetic nerve activity [4], by LFSP power [2] and by the LFRR/HFRR ratio [8]; augmented vagal activity as indicated by the increase of HFRR power [2,3,8], associated with HR reduction [2,3,4,8,9]; decreased stroke volume [2,9]; vasoconstriction due to a local effect [7,9], which has recently been considered the primary effect of hyperoxemia [1], eliciting an increase in peripheral resistance [2,3] and decreased blood flow to the limbs [4]. However, contradictory effects of hyperoxia have also been reported: reduction [6], no change [4] or increase [3] of AP; no change of BRS evaluated by alpha technique [7], and, when estimated by sequence analysis, increase [3] or reduction [2]; and either no change, decrease or increase of PV [5].…”

Section: Discussionmentioning

confidence: 99%

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Beat:To:Beat Autonomic Cardiovascular Response to Short:Term 100%O2 Breathing: a Time:Frequency Analysis Approach

Carrasco-Sosa

Guillen-Mandujano

2016

2016 Computing in Cardiology Conference (CinC)

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In sixteen healthy volunteers, we assessed the effects produced by short-term 100%O2 breathing on the instantaneous time courses of R-R intervals (RR), arterial pressure (AP), arterial oxygen saturation (SaO2), respiratory volume (Res), and, estimated by a time frequency distribution, the high frequency powers of RR (HFRR) and Res (HFRes), the low frequency powers of RR (LFRR) and systolic pressure (LFSP), the LFRR/HFRR ratio, baroreflex sensitivity (BRS) by alpha index and respiratory sinus arrhythmia sensitivity (RSAS IntroductionDespite the extensive therapeutic use of supplemental oxygen in normoxemic and hypoxemic patients [1], which is not risk-free, the reported autonomiccardiovascular effects of 100%O2 breathing in healthy subjects are not consistent. On the one hand, there is consensus that hyperoxia directly causes vasoconstriction [1], vagal activity increase with heart rate (HR) reduction [2,3] and sympathetic activity decrease [2,4]; but on the other hand, contradictory effects of hyperoxia on pulmonary ventilation (PV) [5], arterial pressure (AP) [3,6] and baroreflex sensitivity (BRS) [2,3,7] have been reported. Apparently, hyperoxia produces various effects on different organs in a parallel manner, directly, and separately [1]. Moreover, the participation of either the baroreflex or the respiratory sinus arrhythmia (RSA) mechanisms in these effects remains unclear. Additionally, spectral analysis of cardiovascular variability under hyperoxemic conditions has only been performed using steady-state techniques [2,3,7,8], so the transient changes of the autonomic-cardiovascular variables in the first minutes of hyperoxemia are still unknown. To clarify these issues, by using a timefrequency spectral analysis approach, we assessed the instantaneous time course of the effects produced by short-term 100%O2 breathing on the spectral measures of heart rate variability (HRV) and systolic pressure variability, BRS, RSA sensitivity (RSAS), R-R intervals (RR), AP and respiratory variables. Methods SubjectsSixteen healthy, normotensive and sedentary subjects, 8 men and 8 women, were studied. Their mean age, height and weight were 22.3±1.7 years, 163.2±6.4 cm and 61.6±9.6 kg respectively. Their written informed consent was requested to participate. The present study was approved by the ethics committee of our university. ProtocolVolunteers visited the laboratory twice. The first time, their health status and anthropometric variables were evaluated, and in the second visit the experimental stage was carried out. It consisted of 1-min control (air breathing), 2-min maneuver during which the subjects, with occluded nose, breathed 100%O2 gas stored in a Douglas bag through a non-rebreathing valve (Hans Rudolph), followed by 1.5-min recovery breathing air.ECG, AP, arterial oxygen saturation (SaO2), expired CO2 concentration, and respiration (Res) were recorded throughout the entire study.

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Section: Discussionmentioning

confidence: 99%

“…Because the effects of hyperoxemia are potentially harmful to the heart and vessels [1,3,9] and the risk of organic damage is proportional to the exposure time, in this study we limited 100%O2 breathing to a few minutes.…”

Section: Discussionmentioning

confidence: 99%

Beat:To:Beat Autonomic Cardiovascular Response to Short:Term 100%O2 Breathing: a Time:Frequency Analysis Approach

Carrasco-Sosa

Guillen-Mandujano

2016

2016 Computing in Cardiology Conference (CinC)

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“…Several animal and clinical studies have shown that hyperoxia induces vasoconstriction in the brain, heart, and other tissues [2,7,8]. Hyperoxia can also exacerbate cardiovascular performance and induce cardiac hypertrophy and arrhythmias [9,10], for review see [11]. Therefore, medical uses of NBO or HBO treatments are controversial, and current guidelines recommend limiting exposure to excessively high oxygen concentrations [12].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, medical uses of NBO or HBO treatments are controversial, and current guidelines recommend limiting exposure to excessively high oxygen concentrations [12]. Although molecular mechanisms of protective and adverse effects of hyperoxia are still not well understood, it is widely recognized that increased oxidative stress plays a principal role [2,11]. Increased formation of reactive oxygen (ROS) and nitrogen (RNS) species leads to changes in intracellular redox state and modulation of cell signaling pathways, resulting in alterations in gene expression.…”

Section: Introductionmentioning

confidence: 99%

“…Data from both experimental and clinical studies suggest that beneficial effects of NBO or HBO treatment on brain or heart could be due to increased expression of antioxidant, anti-inflammatory, and anti-apoptotic proteins and reduced production of pro-oxidant, pro-inflammatory pro-apoptotic proteins [ [13][14][15], for review see [2]. However, this is in contrast with studies, which showed that hyperoxia increases cellular oxidative damage [16], for review see [11].…”

Section: Introductionmentioning

confidence: 99%

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Proteomic analysis of mitochondrial proteins in the guinea pig heart following long-term normobaric hyperoxia

et al. 2017

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Normobaric hyperoxia is applied for the treatment of a wide variety of diseases and clinical conditions related to ischemia or hypoxia, but it can increase the risk of tissue damage and its efficiency is controversial. In the present study, we analyzed cardiac mitochondrial proteome derived from guinea pigs after 60 h exposure to 100% molecular oxygen (NBO) or O enriched with oxygen cation (NBO+). Two-dimensional gel electrophoresis followed by MALDI-TOF/TOF mass spectrometry identified twenty-two different proteins (among them ten nonmitochondrial) that were overexpressed in NBO and/or NBO+ group. Identified proteins were mainly involved in cellular energy metabolism (tricarboxylic acid cycle, oxidative phosphorylation, glycolysis), cardioprotection against stress, control of mitochondrial function, muscle contraction, and oxygen transport. These findings support the viewpoint that hyperoxia is associated with cellular stress and suggest complex adaptive responses which probably contribute to maintain or improve intracellular ATP levels and contractile function of cardiomyocytes. In addition, the results suggest that hyperoxia-induced cellular stress may be partially attenuated by utilization of NBO+ treatment.

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Impact of hyperoxia on cardiac pathophysiology

Rodgers

Iyer

Rodgers

et al. 2019

Journal Cellular Physiology

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Mechanical ventilation with high oxygen therapy (hyperoxia) is widely implemented in critical care and ICU settings. Although supplemental oxygen is beneficial to treat hypoxia, its use is also associated with poor outcomes and high mortality in patients. Lung injury due to hyperoxia exposure has been well‐documented in patients, including in adults and neonates. Thus, lung injury due to hyperoxia has been extensively researched in both preclinical and clinical studies. However, hyperoxia has also been shown to be associated with hemodynamic changes in patients in ICU, including reductions in heart rate, stroke volume, and cardiac output. In addition, certain experimental studies report that hyperoxia exposure in neonates results in cardiac dysfunction in later adult life. Despite this, until recently, the impact of hyperoxia within the heart has not been well studied, or reported, specifically in adult experimental models. To close this significant gap, our lab has sought to clarify hyperoxia‐induced cardiac pathophysiology in adult murine models. This review discusses the current findings regarding the cardiovascular impact of hyperoxia exposure.

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Cardiovascular effects of hyperoxia during and after cardiac surgery

Cited by 58 publications

References 109 publications

Beat:To:Beat Autonomic Cardiovascular Response to Short:Term 100%O2 Breathing: a Time:Frequency Analysis Approach

Beat:To:Beat Autonomic Cardiovascular Response to Short:Term 100%O2 Breathing: a Time:Frequency Analysis Approach

Proteomic analysis of mitochondrial proteins in the guinea pig heart following long-term normobaric hyperoxia

Impact of hyperoxia on cardiac pathophysiology

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