Survival to discharge for an out-of-hospital cardiac arrest (OHCA) in England is 7.3% (NHS England, 2022) in comparison with the rest of Europe which is 11.7% (Yan et al, 2020), according to the most recent data available at the time of writing.
Some of this could be attributed to different structures in the emergency services, but there are European countries, such as Switzerland, where the structure is similar to that in the UK ambulance service (Schmutz et al, 2022). There is clearly scope to improve the survival rate after an OHCA in England.
While many aspects of a resuscitation are crucial in the chain of survival (Perkins et al, 2015), such as early chest compressions and early access to a defibrillator (Perkins et al, 2015), post-resuscitation care is more novel, having been introduced by the European Resuscitation Council (ERC) in 2010 (Nolan et al, 2015).
After return of spontaneous circulation (ROSC), post-cardiac arrest syndrome can occur (Association of Ambulance Chief Executives (AACE), 2019). This is because of prolonged, full-body ischaemia; its deleterious effects include anoxic brain injury, myocardial dysfunction, a systemic ischaemia/reperfusion response and persistent precipitating pathology (Stub et al, 2011).
While there are clear prehospital guidelines for clinicians to follow during a resuscitation (AACE, 2019), prehospital guidelines for minimising the incidence of post cardiac arrest syndrome are more generic and consist mainly of monitoring the patient (AACE, 2019).
The most recent Joint Royal Colleges Ambulance Liaison Committee (JRCALC) guidelines (AACE, 2019) simply state that peripheral oxygen saturations should be maintained in the range of 94–98% after the ROSC. In theory, this should be a simple task but peripheral oxygen saturations are often inaccurate and unreliable (Nolan et al, 2015).
Currently, JRCALC guidelines do not consider the risks of saturations falling outside 94–98% or where peripheral capillary oxygen saturations cannot be obtained. The JRCALC guidelines do mention the organ failure and immunological pathway activation that can occur through reperfusion after an ischaemic injury but give no indication on how to lessen this damage in the immediate post-ROSC phase (AACE, 2019). This leaves frontline paramedics with little direction or clarity on the best clinical care for their patient and the impact that over-oxygenation may have after ROSC.
Recently, it has been suggested that hyperoxaemia may play a crucial role in worsening post-cardiac arrest syndrome by increasing free-radical production, which leads to cellular and neuronal injury and apoptosis (Janz et al, 2012; Nelskylä et al, 2013).
Even in healthy volunteers, systemic changes, such as a decrease in peripheral perfusion, have been found in response to hyperoxaemia (Orbegozo Cortés et al, 2015). In a patient experiencing post-cardiac arrest syndrome, these changes may be more dramatic.
The oxygen administered to a patient after ROSC is easily modifiable, and avoiding hyperoxaemia may improve patient outcomes (Janz et al, 2012).
Unfortunately, there are no data for the UK, but an Australian study found that 65% of patients who experienced ROSC after an OHCA arrived at hospital hyperoxaemic (Nelskylä et al, 2013). This suggests that hyperoxaemia could be affecting a large proportion of post-ROSC patients.
To determine clinical hypoxaemia, normoxaemia and hyperoxaemia, arterial blood gases (ABGs) are required as they can be used to measure the partial pressure of oxygen (PaO2) in arterial blood (Mosby's Medical Dictionary, 2017).
In general, hypoxaemia is defined as arterial PaO2<60 mmHg (Bellomo et al, 2011; Oh et al, 2014) and hyperoxaemia as arterial PaO2>300 mmHg (Bellomo et al, 2011; Nelskylä et al, 2013; Oh et al, 2014). Therefore, in normoxaemia, PaO2 is 60–300 mmHg.
Prehospital blood gas analysis provides useful information for the treatment of patients (Jousi et al, 2010). However, to obtain an ABG, a physician is required (Jousi et al, 2010); it was not part of the UK paramedic skill set at the time of writing. Therefore, peripheral oxygen saturation (SpO2) is used to measure patients' oxygenation in the prehospital setting.
Since the 2010 ERC guidelines, when post-resuscitation care was introduced, hyperoxaemia after ROSC has come under increasing scrutiny (Nolan et al, 2015). The 2015 ERC and European Society of Intensive Care Medicine guidelines highlight the significant heterogeneity found in the literature regarding hyperoxaemia after ROSC (Nolan et al, 2015).
They summarise that hypoxaemia should be avoided and that oxygen should not be titrated until a reliable arterial oxygen saturation has been obtained (Nolan et al, 2015). This is in contrast with the JRCALC guidelines, which suggest titration in the range of 94–98% using a peripheral saturation probe (AACE, 2019). This lack of consistency between guidelines could explain why survival-to-discharge differ between the UK and in similarly developed countries.
Therefore, this literature review will critique in detail the current available research to determine if there are detrimental effects of hyperoxaemia in the immediate post-ROSC period in adults who have experienced an OHCA.
Methodology
This literature review has limitations. A systematic review was not possible because of financial restraints. However, by following a detailed methodology and recording the steps taken, a valid conclusion to the research question can be reached (Aveyard et al, 2015).
Table 1 shows the databases used when searching for relevant literature and the rationale for including each one. By using a variety of databases, a larger proportion of all evidence on the topic can be found and a more objective search is created.
| Database | Description | Rationale |
|---|---|---|
| PubMed | Provides free access to a database of medical, nursing, dental, veterinary, healthcare and preclinical sciences journal articles (National Library of Medicine, 2022) | PubMed (2022) contains more than 34 million citations and therefore covers a wide range of literature so minimises bias |
| Cumulative Index to Nursing and Allied Health Literature (CINAHL) | Provides indexing of nursing and allied health literature along with books and some grey literature, such as nursing dissertations (EBSCO Health, 2022a) | CINAHL is more subject specific than PubMed but still provides access to a large number of records and journals |
Medline, a database holding journal articles in life sciences and medicine, was not searched as PubMed provides access to it (National Library of Medicine, 2022), so searching it would produce duplicate results.
Limitations of the search included not being able to access the full text of an article without a subscription to the journal, which has financial implications. Articles not published in English were excluded from the search (Table 2) as translation may lead to misinterpretation.
| Database | Limits set | Key search terms | Number of results |
|---|---|---|---|
| PubMed | Published in the last 10 years |
(hyperox*) AND (ROSC or return of spontaneous circulation or post-arrest) | 46 |
| Published in the last 10 years |
(resuscitation OR rosc OR return of spontaneous circulation) AND (hyperox*) AND (normox*) AND (animal) AND (oxygen) NOT (paediatric or pediatric or neonate or neonatal or new born) | 14 | |
| CINAHL | Publication between 2012 and 2022 |
(hyperox*) AND (ROSC or return of spontaneous circulation or post-arrest) | 22 |
| Publication between 2012 and 2022 |
(resuscitation OR rosc OR return of spontaneous circulation) AND (hyperox*) AND (normox*) AND (animal) AND (oxygen) NOT (paediatric or pediatric or neonate or neonatal or new born) | 7 | |
| Publication between 2012 and 2022 |
(hyperoxia OR hyperoxaemia) AND (reactive oxygen species OR lung damage) NOT (paediatric OR children OR neonates OR neonatal OR new born OR newborn) | 35 | |
| Publication between 2012 and 2022 | resuscitation rosc return of spontaneous circulation hyperoxia hyperoxemia hyperoxaemia normoxia oxygen | 7 | |
| Publication between 2012 and 2022 | hyperoxia hyperoxemia hyperoxaemia reactive oxygen species lung damage | 36 |
When searching for primary literature, Boolean operations were used in PubMed and CINAHL. Boolean operations allow a narrower search to be carried out by using key words and excluding criteria that are not wanted (Aveyard et al, 2015; EBSCO Help, 2022b).
This literature review focused on adult patients only. The reasoning behind this is that neonates and young children have significantly different physiology, resulting in different responses to the same SpO2 and PaO2 measures (Eastwood et al, 2016). To exclude irrelevant articles, words such as ‘children’, ‘new born’ and ‘neonates’ were used as exclusion criteria.
The search terms used in each database and the number of results are shown in Table 2. The results found only two randomised controlled trials (RCTs) where human populations had been studied (Kuisma et al, 2006; Young et al, 2014).
RCTs have long been considered the most accurate method of establishing a cause-and-effect relationship by comparing a treatment group with a control group (Sibbald and Roland, 1998) and are designed to minimise bias through a double-blind design (Levin, 2007).
The disadvantages of RCTs include the requirement of previous knowledge to design an effective study and, in healthcare, there can be significant ethical issues with withholding treatment to control groups (Levin, 2007).
Several relevant retrospective studies on humans who had experienced a cardiac arrest were identified. Retrospective studies can produce strong evidence as it is possible to collect data from a large number of patients and there is little bias involved as patients do not choose or are not chosen to enter the study, but are entered into it when they meet the criteria (Anthonisen, 2009). There are also fewer ethical concerns as patients are not treated differently for research purposes (Euser et al, 2009).
On the other hand, the data needed for the study may not be collected at the same time point for each patient, and some data may be missing. It is also not possible to control a variable to elucidate a response (Anthonisen, 2009).
Although different databases were searched, many of the results were found in multiple databases (Table 2), so fewer results than expected were yielded.
Kuisma et al (2006) published their research before the 10-year cut-off; this study was found through the references of a systematic review of the effect of hyperoxia on survival following adult cardiac arrest (Wang et al, 2014). This process of searching references for further relevant articles is called snowballing and allows for a much more thorough identification of evidence (Aveyard et al, 2015). This process was used throughout the literature search.
Literature was selected if it was relevant to the research question and findings could be applied to the prehospital setting. The critique framework by LoBiondo-Wood and Haber (2002) was applied as it was developed specifically for healthcare research.
The findings from each piece of literature chosen will be discussed to deduce if paramedics can improve patients' outcome by avoiding hyperoxaemia after a successful resuscitation.
Effect of post-ROSC hyperoxaemia
Much of the literature found concludes there is a negative or neutral association with hyperoxaemia after a successful resuscitation.
A neutral association is one where being hyperoxaemic confers no advantage or disadvantage to post-ROSC patients compared with being normoxaemic. A negative association could be a decrease in survival to discharge or an increase in neurological injury (Oh et al, 2014).
The hypothesis behind hyperoxaemia causing damage is through cerebral and myocardial vasoconstriction (Janz et al, 2012), altered cellular metabolism and an increase in the production of reactive oxygen species leading to apoptosis of cells and neurones (Nelskylä et al, 2013; Orbegozo Cortés et al, 2015). The effects of this can lead to worsening neurological injury and possibly death (Bellomo et al, 2011).
A positive association with post-ROSC hyperoxaemia could be an increase in survival to discharge or a decrease in organ failure (Christ et al, 2016). Resuscitation itself is more successful with 100% oxygen and, as PaO2 increases, so do ROSC rates (Spindelboeck et al, 2013). The relationship between PaO2 and survival to discharge in post-ROSC patients may follow a similar pattern.
Therapeutic hypothermia
In England, therapeutic hypothermia (TH) is recommended by National Institute for Health and Care Excellence (NICE) (2011) guidelines.
TH involves reducing the patient's core temperature to 32–34°C to decrease neurological injury after resuscitation. Evidence suggests that neurological damage is the biggest cause of death after an OHCA (Elmer et al, 2015), and the Resuscitation Council UK advises targeted temperature management for any adult patient who remains unresponsive after ROSC (Nolan et al, 2021). Therefore, it is possible that many OHCA patients will undergo TH.
Janz et al (2012) carried out an analysis on patients who had survived a cardiac arrest and went on to be treated with TH. They found that after TH, patients who had been hyperoxaemic had higher mortality rates and worse neurological function than those who had not been hyperoxaemic. The analysis was carried out once patients were in hospital and the study methods did not differentiate between whether patients had a cardiac arrest in or out of hospital (Janz et al, 2012). This could affect the results as the aim of TH is to reduce neurological damage (NICE, 2011), which is the biggest cause of death after an OHCA but not an in-hospital cardiac arrest (IHCA) (Elmer et al, 2015).
There was no significant difference between the two groups regarding time spent under TH but survivors were generally younger and had a shorter time to ROSC, which could affect results (Janz et al, 2012). These differences suggest a larger study with differentiation between IHCA and OHCA to increase validity is needed before conclusions can be drawn (Roberts et al, 2006).
One of the two RCTs that investigated hyperoxaemia compared patients who received 30% oxygen with patients who were given 100% oxygen after an OHCA. Kuisma et al (2006) analysed the results by subgroup and, in contrast to Janz et al (2012), did not find higher rates of mortality or increased markers of neurological damage in those with hyperoxaemia and TH in comparison to normoxic patients who underwent TH.
This could be because of differences in study design, as Kuisma et al (2006) looked at serum markers while Janz et al (2012) used clinical outcomes. Furthermore, the studies were conducted 6 years apart, so medical advances may lead to discrepancies.
Kuisma et al (2006) found that hyperoxaemic patients who did not undergo TH had higher levels of markers for neuronal injury than normoxic patients who were not treated with TH. Therefore, TH may act in a protective manner against the damaging effects of hyperoxaemia.
Hyperoxaemia and PaO2 threshold
The widely-accepted threshold for hyperoxaemia is arterial PaO2>300 mmHg and many research papers classify patients in line with this assumption (Bellomo et al, 2011; Nelskylä et al, 2013; Oh et al, 2014). This value may be appropriate for a healthy individual, but post-ROSC patients may be sensitive to an arterial PaO2<300 mmHg.
The study design by Elmer et al (2015) allowed this value to be questioned. Patients' PaO2 measurements were assigned a value ranging from 0 (normoxia) to 2 (severe hyperoxaemia) every hour, resulting in a single score after a 24-hour period. This composite score allows the inclusion of patients who would otherwise have fallen into different categories at different times.
During analysis, variables such as location where the cardiac arrest occurred, initial rhythm, age and less responsive care were controlled for (Elmer et al, 2015). This reduced the number of variables that cannot be controlled in a retrospective study and helped to single out oxygenation status as a cause of mortality.
Elmer et al (2015) found that patients with moderate hyperoxia (PaO2=101–299 mmHg) over the first 24 hours after ROSC had better organ function than normoxic patients (PaO2=60–100 mmHg), but those with severe hyperoxia (PaO2>300 mmHg) had higher mortality rates, supporting hyperoxaemia as PaO2>300 mmHg.
Previously, worse organ function at 72 hours after ROSC has been associated with poorer survival after cardiac arrest (Elmer et al, 2015) so Elmer et al's (2015) findings could have clinical significance regarding long-term survival. Elmer et al (2015) deduced from the results that negative outcomes occur once PaO2 exceeds a threshold; however, the value of this needs to be investigated further. Unfortunately, long-term and neurological outcomes were not reported, which means a further study is required to investigate these.
Janz et al (2012) also designed a study that did not use >300 mmHg as a classification of hyperoxaemia, choosing instead to analyse PaO2 as a continuous variable rather than dividing patients into hyperoxaemic and non-hyperoxaemic groups. The results showed that survivors had a median PaO2 of 198 mmHg and non-survivors a median PaO2 of 254 mmHg, which does not exceed the generally accepted value for hyperoxaemia (Janz et al, 2012). Patients with a poor neurological outcome also did not reach a median PaO2 >300 mmHg; the median PaO2 was 264.5 mmHg compared with a median of 197 mmHg for the group of patients who had a favourable neurological outcome (Janz et al, 2012). This, again, brings into question the level at which PaO2 becomes harmful.
While patients may be deemed to be hyperoxaemic at a certain time point, any detrimental effects this has may depend on how soon this occurs after ROSC. Oh et al (2014) focused on the early post-ROSC period by taking an ABG 10 minutes after ROSC and a second ABG 60–120 minutes after ROSC. They found no correlation between early hyperoxaemia and survival to discharge or neurological outcome.
All the patients in Oh et al's (2014) study had experienced an IHCA, so caution must be taken when applying this knowledge to the prehospital area as the results may not be the same for an OHCA.
Nelskylä et al (2013) looked at patients who had ABGs taken up to 24 hours after ROSC. A time of 24 hours after ROSC is not directly relevant to paramedics but the results did show higher blood glucose levels in patients who had been exposed to hyperoxaemia (a median of 13.8 mmol/l versus 10.5 mmol/l for normoxic patients) (Nelskylä et al, 2013).
Blood glucose is generally used as a measure of stress response after a cardiac arrest (Nelskylä, et al, 2013) and could indicate that hyperoxaemia is putting the body under increased stress.
The raised blood glucose could also have resulted from a prolonged resuscitation time (Nelskylä et al, 2013), but there is no data linking individual blood glucose levels to the time taken to achieve ROSC or between patients who experience an IHCA or an OHCA (Nelskylä et al, 2013). Therefore, no conclusion on the cause of the raised blood glucose levels can be reached.
Perhaps the most relevant piece of research to be considered is by Wang et al (2017) where 9176 adult OHCA patients were studied across multiple sites in the United States. This focused study found that any significant abnormality in oxygen levels was detrimental to patients and had an impact on survival to discharge. Both shockable and non-shockable rhythms were included and adjusted for, making the study generalisable to the wider adult population.
In contrast to Oh et al (2104), Wang et al (2017) found that hyperoxaemia at any time point was harmful. However, caution must be taken when directly comparing the two studies as the ABG was taken within 1 hour of arriving at hospital in the study by Wang et al (2017); depending on the geographical location when ROSC was achieved, there could be vastly different times since ROSC for individual patients.
A more recent study found no association between hyperoxaemia and 1-year mortality (Humaloja et al, 2019). However, this study included both IHCA and OHCA and was smaller, with only 1110 patients included, 699 of whom had had an OHCA. One-year mortality was a secondary outcome, with the main focus of the research being on neurological outcome. It is also impossible to compare survival to discharge (the outcome studied by Wang et al (2017)) and 1-year mortality, as Humaloja et al (2019) did not consider other causes of death in that 1-year time period that may be unrelated to the cardiac arrest.
Discussion
Hyperoxaemia may worsen damage caused through reperfusion, confounding the neurological damage after a cardiac arrest. The reperfusion stage of the brain is potentially more important after an OHCA than an IHCA as evidence suggests that neurological damage is the biggest cause of death after an OHCA (Elmer et al, 2015). Therefore, improving neurological status should be a target to increase the survival to discharge after an OHCA.
Currently, TH is used in an attempt to reduce neurological damage after a resuscitation (NICE, 2011). Yet even when TH is used, patients who have been hyperoxaemic have an increased mortality rate and worse neurological outcome than normoxic patients (Janz et al, 2012). In these patients, their arterial PaO2 was not even above the generally accepted value of >300 mmHg for hyperoxaemia. Patients with higher mortality rates had a mean arterial PaO2 of 254 mmHg, and those with a negative neurological outcome had a mean arterial PaO2 of 264.5 mmHg (Janz et al, 2012). One suggestion is that arterial PaO2>300 mmHg is not the correct cut-off for hyperoxaemia in the post-ROSC patient and it may be closer to the median values found by Janz et al (2012).
Exposure to moderate hyperoxaemia (arterial PaO2=101–299 mmHg) has been linked to improved organ function, yet severe hyperoxaemia (arterial PaO2>300 mmHg) leads to an increase in mortality (Elmer et al, 2015). Therefore, it could be that hyperoxaemia is beneficial until a critical level is reached.
The body has endogenous antioxidants, which can counteract low levels of oxidative stress (Rizzo et al, 2010; Elmer et al, 2015). During a cardiac arrest, resuscitation and ROSC, reactive oxygen species are produced and subsequently removed by these endogenous antioxidants, diminishing the antioxidants present in the human body (Elmer et al, 2015). Further production of reactive oxygen species because of hyperoxaemia could overwhelm the remaining antioxidants, resulting in negative outcomes because of the damaging reactive oxygen species.
The exact level of hyperoxaemia a patient can tolerate may vary depending on the level of endogenous antioxidants present. As these are depleted during a resuscitation, patients with a longer resuscitation will be more sensitive to hyperoxaemia, so the traditional value for hyperoxaemia may be much higher than the level the patient can tolerate.
Janz et al (2012) found that survivors generally had a shorter time to ROSC and it is possible this is partially because of less depletion of endogenous antioxidants, allowing the patient to be more protected from reactive oxygen species caused by hyperoxaemia. Because of the generally longer time to ROSC in OHCA than IHCA patients (Kuisma et al, 2006; Oh et al, 2014), hyperoxaemia may be more damaging after an OHCA than an IHCA. If the above hypothesis is correct, it is imperative that paramedics do not cause hyperoxaemia in OHCA post-ROSC patients to improve patients' outcome.
The improved organ function with moderate hyperoxaemia found by Elmer et al (2015) could be through mechanisms such as improved mitochondrial function and less nitro-oxidative stress, which have been found using animal models of cardiac arrest (Yeh et al, 2012). Elmer et al (2015) found an improved Sequential Organ Failure Assessment (SOFA) score at 24 hours post-ROSC with hyperoxaemia. While this piece of research did not look at long-term survival, the SOFA score is a good predictor of death after discharge from intensive care (Matsumura et al, 2014). Therefore, the study suggests that moderate hyperoxaemia is beneficial to post-ROSC patients. Even if hyperoxaemia cannot improve survival to discharge, this is not the only important factor in post-ROSC patients. Length of stay in hospital and the resulting quality of life that the patient has are also significant and the research by Elmer et al (2015) suggests that hyperoxaemia may be able to alter these factors.
Because of the nature of their work, paramedics are generally concerned with hyperoxaemia occurring for up to 1 hour after ROSC. Immediately after ROSC, during the initial reperfusion phase, autoregulation of cerebral blood flow can be impaired, which can lead to a secondary cerebral injury due to hypoxaemia (Oh et al, 2014). On the other hand, reactive oxygen species resulting from hyperoxaemia can also cause cerebral injury (Elmer et al, 2015). Different researchers have looked at hyperoxaemia at different time points during patients' recovery, yet both of these studies found no significant difference in survival to discharge between hyperoxaemic patients and normoxaemic patients.
Humaloja et al's (2019) research also found no significant difference but considered 1-year mortality and was a small study. Oh et al (2014) focused on early hyperoxaemia but looked only at IHCA patients. As survivors of IHCA and OHCA have different causes of death before discharge (Elmer et al, 2015), their physiology may differ. For this reason, the inconclusive results from Oh et al (2014) cannot be generalised to the OHCA post-ROSC patient. Nelskylä et al (2013) looked at hyperoxaemia within the first 24 hours of ROSC. There was no difference between OHCA and IHCA patients, which could have led to no significant effect of hyperoxaemia being found as these two patient groups may require different treatments. The data need to be analysed in more depth to allow associations for different populations to be made, especially as hyperoxaemia was more common in the OHCA patient group (Nelskylä et al, 2013).
More recently, Wang et al (2017) found that any hyperoxaemia in the first 24 hours after ROSC increased mortality, regardless of the time at which it happened. This study is more current than the others discussed, and included a large study population that was focused on OHCA so can be considered the most valid piece of research when determining whether hyperoxaemia resulting from excessive oxygen administered by paramedics post-ROSC is damaging to a patient's clinical outcome.
With regards to clinical measures such as lactate, pH and glucose, the only significant difference between hyperoxaemic patients and non-hyperoxaemic patients was in blood glucose levels (Nelskylä et al, 2013). Blood glucose was found to be higher in hyperoxaemic patients, which could suggest a stress response (Nelskylä et al, 2013).
As this result was found in a retrospective study, only an association can be concluded. A cause-and-effect relationship needs to be proved before hyperoxaemia can be said to be the cause of increased blood sugar and subsequent stress on the body. Causes such as a prolonged OHCA need to be ruled out, as this may also induce a greater stress response, which is reflected in a patient's blood glucose level.
As paramedics will be in charge of the early post-ROSC patients' care after an OHCA—generally within the first 60 minutes—these data are important to consider as a titration of oxygen may decrease the survival to discharge rates currently seen in the UK.
Conclusion
This literature review has discussed both the positive and negative effects of hyperoxaemia on the post-ROSC patient, and some of the possible mechanisms behind this.
While there are gaps in the research, hyperoxaemia may benefit the post-ROSC patient up to a certain level (Elmer et al, 2015). Once the reactive oxygen species produced by hyperoxaemia overwhelm the patient's endogenous antioxidants, harm may begin to occur (Rizzo et al, 2010). This would suggest that in the relatively short time period that paramedics will spend with a post-ROSC patient, there is no need to reduce the oxygen administered.
For more knowledge to be gained in post-ROSC hyperoxaemia after an OHCA, the following are recommendations for future research:
Currently, paramedics should ensure adequate oxygenation is given to a patient after ROSC. While short periods of hyperoxaemia appear to be beneficial to a post-ROSC patient, after an extended resuscitation, endogenous antioxidants may easily be overwhelmed. If a reliable oxygen saturation reading can be obtained, then the paramedic may wish to titrate the patient's oxygen levels to an SpO2 of 94–98% to prevent damaging reactive oxygen species. As long as hypoxia is avoided, no damage will be done.
Once future research provides more robust evidence on the oxygenation requirements of a post-ROSC patient who has experienced an OHCA, it is important that both prehospital and in-hospital care are able to provide this to achieve the best patient outcome possible.