Effect of Hyperoxia on Left Ventricular Function and Filling Pressures in Patients With and Without Congestive Heart Failure

Mak, Susanna; Azevêdo, Eduardo Ribeiro de; Liu, Peter P.; Newton, Gary E.

doi:10.1378/chest.120.2.467

Cited by 153 publications

(114 citation statements)

References 33 publications

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“…22 It has been demonstrated that hyperoxia may influence systemic vascular resistance, stroke volume and BP. 23,24 Thus, the lack of blood-pressure decrease during chemoreflex deactivation can be explained by local vasoconstricting effect of hyperoxia that could offset the sympathoinhibitory effect of chemoreceptor deactivation. To clarify the influence of carotid body deactivation on the circulatory parameters in hypertensive patients, a more detailed hemodynamic approach including cardiac output measurement would need to be applied.…”

Section: Discussionmentioning

confidence: 99%

“…The circulatory effects of hyperoxia were described in healthy subjects and patients with heart failure. 23,24 Long periods of breathing 100% oxygen increased systemic resistance, decreased stroke volume and impaired left ventricular relaxation. It has been shown in the animal model 27 that shorter periods of hyperoxia inhibit ventilatory and circulatory chemoreflex response.…”

Section: Discussionmentioning

confidence: 99%

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Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

et al. 2011

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Carotid chemoreceptors provoke an increase in muscle sympathetic nerve activation (MSNA) in response to hypoxia; they are also tonically active during normoxic breathing. The contribution of peripheral chemoreceptors to sympathetic activation in hypertension is incompletely understood. The aim of our study was to investigate the effect of chemoreceptor deactivation on sympathetic activity in untreated patients with hypertension. A total of 12 untreated hypertensive males and 11 male controls participated in this randomized, crossover, placebo-controlled study. MSNA, systolic blood pressure(BP), diastolic BP, heart rate (HR), electrocardiogram, hemoglobin oxygen saturation (Sat%) and respiratory movements were measured during repeated 10-min periods of respiration with 100% oxygen or 21% oxygen in a blinded fashion. Compared with controls, hypertensives had higher resting MSNA (38±10 vs. 29±0.9 burst per min, Po0.05), systolic BP (150±12 vs. 124±10 mm Hg, Po 0.001) and diastolic BP (92 ± 10 vs. 77 ± 9 mm Hg, Po0.005). Breathing 100% oxygen caused significant decrease in MSNA in hypertensive patients (38 ± 10 vs. 26 ± 8 burst per min and 100 ± 0 vs. 90 ± 10 arbitrary units, Po0.05) and no change in controls (29±9 vs. 27±7 burst per min and 100±0 vs. 96±11 arbitrary units). BP, respiratory frequency and end tidal CO 2 did not change during chemoreceptor deactivation with hyperoxia. HR decreased and Sat% increased in both the study groups. These results confirm the role of tonic chemoreceptor drive in the development of sympathetic overactivity in hypertension.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

et al. 2011

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“…24 In addition, supplemental oxygen has been suggested to cause hyperoxia, which can have an adverse effect on myocardial function because of the generation of oxygen free radicals. 25,26 We previously conducted a prospective study to elucidate the efficacy of 12 weeks of nocturnal oxygen therapy using a conventional oxygen concentrator on ventricular function, severity of HF, and QOL, together with an improvement in SDB, in ambulatory patients with stable CHF and CSR. 19 That study demonstrated that short-term treatment with nocturnal oxygen significantly improved NYHA functional class, Specific Activity Scale as a measure of QOL, and SDB in CHF patients with CSR-CSA; LVEF also increased from baseline to the end of the study.…”

Section: Discussionmentioning

confidence: 99%

Improvement of Quality of Life With Nocturnal Oxygen Therapy in Heart Failure Patients With Central Sleep Apnea

Sasayama

Izumi

Matsuzaki

et al. 2009

Circ J

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“…[99][100][101] Kilgannon et al 63 have demonstrated that hyperoxia played a greater role in mortality than did hypoxia following cardiac arrest. A number of other investigations and meta-analyses 102-107 on this subject have been published following the work of Kilgannon.…”

Section: Myocardial Infarction/cardiac Arrestmentioning

confidence: 99%

Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients?

Kallet

Branson

2016

Respir Care

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Oxygen is both lifesaving and toxic. Appropriate use of oxygen aims to provide a balance between the two effects. Although local oxygen toxicity to the lung is well accepted, recent evidence has called into question the negative consequences of hyperoxemia in other organ beds. Hyperoxia following cardiac arrest, traumatic brain injury, and stroke has been shown to worsen outcomes. The role of hyperoxemia in mechanically ventilated patients, in the face of non-toxic inspired oxygen concentrations, is less clear. This paper will review the data for and against the use of conservative oxygen targets and the avoidance of hyperoxemia in mechanically ventilated patients. Key words: hyperoxia; hyperoxic acute lung injury; lung protective ventilation; oxygen toxicity; reactive oxygen species; ventilator-induced lung injury. [Respir Care 2016;61(6):801-817.

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Effect of Hyperoxia on Left Ventricular Function and Filling Pressures in Patients With and Without Congestive Heart Failure

Cited by 153 publications

References 33 publications

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

Improvement of Quality of Life With Nocturnal Oxygen Therapy in Heart Failure Patients With Central Sleep Apnea

Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients?

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