Oxygen After Cardiac Arrest: Enough Is Enough?
| Autor: | Nicole McKenzie, Geoffrey J. Dobb |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Hyperoxia
medicine.medical_specialty medicine.diagnostic_test business.industry medicine.medical_treatment 030208 emergency & critical care medicine 030204 cardiovascular system & hematology Return of spontaneous circulation medicine.disease medicine.disease_cause Oxygen tension 03 medical and health sciences Pulse oximetry 0302 clinical medicine Physiology (medical) Internal medicine medicine Breathing Cardiology Cardiopulmonary resuscitation medicine.symptom Cardiology and Cardiovascular Medicine business Reperfusion injury Oxidative stress |
| Zdroj: | Circulation. 137:2125-2127 |
| ISSN: | 1524-4539 0009-7322 |
| DOI: | 10.1161/circulationaha.118.033620 |
| Popis: | Article, see p 2114 Return of spontaneous circulation (ROSC) is just the first challenge when a person has a cardiac arrest. At least equally important from a patient perspective are survival to hospital discharge and a good neurological outcome. The 2015 update to the American Heart Association guidelines1 emphasizes the importance in postcardiac arrest care of identification and treatment of the cause of the cardiac arrest and assessment and mitigation of ischemia-reperfusion injury to multiple organs including the brain. The associated systematic review identified 3 observational studies suggesting that hyperoxia may worsen patient outcomes, although 6 other studies, including 1 small randomized controlled trial,2 did not confirm this finding.1 The guideline recommendation is to use the highest possible available oxygen concentration until the arterial oxygen saturation estimated by pulse oximetry (Spo2) or Pao2 can be measured (class IIa, level of evidence C, expert opinion). When these measurements are available, an oxyhemoglobin saturation >94% is recommended. The theoretical basis for avoiding hyperoxia when an ischemia-reperfusion injury is present is strong. Production of reactive oxygen species by mitochondria generally increases with increasing oxygen tension leading to oxidative stress and flow on effects that include damage to nucleic acids, proteins, and lipids; cell death through both apoptotic and necrotic pathways; release of endogenous damage–associated molecular pattern molecules with subsequent mitochondrial damage; and polymorph activation with a systemic inflammatory response.3 Hyperoxia can also induce adverse cardiovascular effects that include reduced coronary blood flow of 8% to 29% in various settings, vasoconstriction, and increased heterogeneity within the microcirculation that reduces oxygen delivery to underperfused tissue.4 A meta-analysis of animal studies modeling cardiac arrest and subsequent cardiopulmonary resuscitation comparing ventilation with 100% oxygen with ventilation with a lower oxygen concentration included 6 studies, and found a significantly … |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|