Research ArticleNew Horizons Symposium

Ventilation and Oxygenation During and After Adult Cardiopulmonary Resuscitation: Changing Paradigms

Ahmed I Algahtani, J Brady Scott and Jie Li
Respiratory Care December 2024, 69 (12) 1573-1586; DOI: https://doi.org/10.4187/respcare.12427

Abstract

Cardiac arrest (CA) remains a major cause of death despite advancements in cardiopulmonary resuscitation (CPR), post–resuscitation care, and international efforts to develop evidence-based guidelines. Effectively managing ventilation and oxygenation during and after CPR is vital for patient survival and neurological outcomes, yet it remains a challenging task. This review examines current strategies for ventilation and oxygenation during and after CPR, focusing on evidence-based guidelines, the balance between ventilation effectiveness and risks, and proposed methods for monitoring ventilation quality. It emphasizes the need to provide adequate ventilation and oxygenation during and after CPR while avoiding hyperventilation and hypoventilation, which can negatively impact resuscitation and post-CA outcomes. The review also explores mechanical ventilation as an alternative to manual methods and the use of feedback devices. The impact of post-CA ventilation and oxygenation on patient outcomes and recommended management strategies are discussed. Finally, the review highlights current gaps in the literature and the need for more well-designed large clinical studies, such as the impact of different ventilation variables (tidal volume and breathing frequency) on the return of spontaneous circulation and long-term outcomes.

Introduction

Cardiac arrest (CA) is a serious, life-threatening medical emergency that claims thousands of lives each year.1,2 The incidence of CA, both in and out of hospital, is a significant challenge for the health care community regarding meaningful recovery and survival.2 Although there have been significant advances in CA care, survival rates remain modest, particularly survival with intact neurological function. This underscores the need for improvement in both cardiopulmonary resuscitation (CPR) and post–resuscitation care.

Global collaboration to enhance the quality of CPR and post–resuscitation care has been ongoing for decades.3 As a result, international CPR and post–resuscitation clinical practice guidelines have been published and frequently updated.3 For patients who experience in-hospital CA (IHCA), adherence to these guidelines has been shown to enhance the quality of CPR, increase the likelihood of survival, and improve neurological function.4 Whereas it is encouraging that guideline adherence improves important outcomes, survival rates after IHCA are still low.4,5

An essential part of the guidelines is the focus on providing safe and effective ventilation and oxygenation during CPR and after the return of spontaneous circulation (ROSC). Yet, most of the recommendations for ventilation and oxygenation are based on a relatively narrow body of evidence, most of which was derived from animal and observational studies.3,6 Some recommendations have remained unchanged over time simply due to the lack of large, well-designed clinical trials.7,8 This review examines current recommended strategies for ventilation and oxygenation during CPR and post-CA and techniques for monitoring delivery to optimize care and patient outcomes. Additionally, areas where additional research could potentially enhance patient outcomes following CA will be identified.

Ventilation and Oxygenation During CPR

Proper ventilation and oxygenation during CPR involve providing optimal gas exchange while minimizing harm.9,10 Excessive ventilation, either by high breathing frequencies, large tidal volumes (VT), or both, can lead to dynamic lung hyperinflation. Dynamic hyperinflation can lead to increased intrathoracic pressures, adversely affecting hemodynamics by decreasing venous return and ultimately diminishing coronary and cerebral perfusion.8,11,12 Also, dynamic hyperinflation increases pulmonary vascular resistance, limiting blood flow to the pulmonary circulation and worsening gas exchange.13 Furthermore, hyperventilation lowers blood CO2 levels, leading to cerebral vasoconstriction and reducing blood flow to the brain.8,13 Excessive VT delivered during bag-mask ventilation (BMV) may lead to gastric inflation and abdominal distention. Gastric inflation and abdominal distention can also increase intrathoracic pressure; however, it is unclear if this impacts ROSC.14,15 Overall, it appears that hyperventilation may impair or delay ROSC and reduce the chance of survival with intact neurological function.8,11-13 Hypoventilation may also be detrimental, as it can lead to hypoxemia, hypercapnia, and acidemia.8,13

Oxygen is essential in sustaining life for all living beings, yet its role in resuscitation is nuanced. Oxygen is necessary for mitochondrial aerobic respiration, facilitating the adenosine triphosphate production, and generating reactive oxygen species.16,17 Adenosine triphosphate provides the energy required for the body to function, while reactive oxygen species play a role in immune responses.16,17 However, high levels of reactive oxygen species can be toxic, leading to direct lung damage, coronary vasoconstriction, reperfusion injury, and poor gas exchange.17 Despite these risks, correcting hypoxia during CPR is crucial, as a high PaO2 appears to enhance the likelihood of ROSC and survival with meaningful neurologic function.18 Also, low blood oxygen levels lead to vasoconstriction of the pulmonary vasculature, limiting blood flow into the pulmonary circulation and left heart, which may reduce the effectiveness of chest compressions.13 In contrast, hyperoxia should be avoided after ROSC as it is associated with increased in-hospital mortality.19

Current Evidence-Based Guidelines and Recommendations

Airway management during CPR.

The most recent updates on airway management during CPR include recommendations supported by evidence varying in strength and certainty (see Table 1).3,9,10,20,-,31 Current CPR guidelines prioritize chest compressions over airway management and ventilation to improve resuscitation outcomes.9,21,25 For basic airway management, the head tilt–chin lift technique is recommended for airway opening in adults unless a cervical spine injury is suspected, in which case a jaw thrust without head extension is preferred.9,21 If the jaw thrust is insufficient for adequate ventilation, the head tilt–chin lift may be used carefully, considering the risk of spinal injury.9,21

View this table:
Table 1.

Summary of Present Evidence-Based Guideline Recommendations for Ventilation and Oxygenation During Cardiopulmonary Resuscitation

Further recommendations include considering BMV or advanced airway interventions for adults in CA. For out-of-hospital CA (OHCA), a supraglottic airway (SGA) is recommended over tracheal intubation for providers with less experience or who have had a low success rate with tracheal intubation.22,26 Conversely, for those with extensive experience and competence with the placement of artificial airways, using either SGA or endotracheal tube is advised, including in IHCA situations.22,26 Waveform capnography is strongly recommended for verifying proper tracheal tube placement and continuous monitoring.10,27 The American Heart Association (AHA) emphasizes the need for regular retraining for providers performing intubation alongside implementing continuous quality improvement initiatives.22 These measures are intended to mitigate complications associated with advanced airway management techniques, such as SGA placement and intubation, and improve success rates.22

The 2019 International Liaison Committee on Resuscitation (ILCOR) Consensus on Science with Treatment Recommendations (CoSTR) for Advanced Life Support (ALS) Task Force identified notable gaps in airway management during CPR. Key areas lacking clarity include the optimal airway management technique for adults with IHCA and the impact of various airway management strategies on oxygenation, ventilation, and no-flow time during CPR.26 Additionally, the task force has emphasized the need for additional research on the impacts of using SGA or tracheal intubation, aside from BMV, on CPR outcomes.26 They also noted a need for further investigation into the clinical training and experience required to achieve and maintain expertise across airway management techniques.26

Ventilation during CPR.

Ventilation during CPR is a dynamic process requiring careful attention to technique, rate, and volume to be effective.21,22 Recently updated guidelines on ventilation during CPR include recommendations of varying strengths, ranging from very low to moderate certainty.3,9,10,20-25 Recommendations vary between providers (layperson or trained health care provider), settings (OHCA or IHCA), and if the cardiac event was witnessed or unwitnessed. For example, CPR guidelines recommend that laypersons provide chest compressions and rescue breaths but only if trained and willing.25 If the laypersons are not trained or willing, the guidelines support compression-only CPR for all patients in CA.25 Recommendations for ventilation by health care providers during CA are (1) VT between 500–600 mL or to ensure visible chest rise, (2) 1-s inspiratory times, and (3) ventilation rates of 10 breaths/min when an advanced airway device is inserted.3,20,21,25 Despite these and other recommendations, a significant gap in clinical research persists regarding the direct impact of these strategies on ROSC and other favorable outcomes.3,20 For example, the optimal VT and ventilation rate during CPR remain unknown.20

Oxygenation during CPR.

AHA and ILCOR CoSTR recommend administering the highest possible oxygen concentration during CPR.20,27 This approach aims to maximize oxygen delivery and reduce risks associated with systemic hypoxemia.20,21 However, specific arterial and tissue oxygen targets and the reliability of ways to monitor and control oxygen targets remain unclear.20 These areas are recognized as significant knowledge gaps, driven at least partially by the limited clinical trials investigating various oxygen concentrations during CPR.20

The AHA and ILCOR guidelines address other oxygenation techniques like passive oxygen insufflation (passive ventilation) and extracorporeal CPR.3,26,27 Currently, the routine use of passive oxygen is not advised for adults undergoing CPR in either the out-of-hospital or in-hospital setting.3 The only exception is emergency medical services systems using bundles of care, which include minimally interrupted cardiac resuscitation strategy or continuous chest compression.9,24,25 Current guidelines suggest that extracorporeal CPR can be considered a rescue intervention when conventional CPR is failing and where its rapid implementation by experienced and skilled providers is possible.3,22,29

The Conundrum of Adequate Ventilation: Rate and Tidal Volumes

The ongoing conundrum over ventilation (rate and VT) during CPR centers on the balance between providing effective ventilation and avoiding hypoventilation and hyperventilation, both of which are harmful during CPR and associated with poor outcomes.11,12,32-35 Several clinical studies, mostly experimental animal studies, have assessed the effect of different ventilation rates during CPR and their impact on outcomes (see Tables 2 and 3).11,12,33-46 Ventilation rates that are too low may lead to poor ventilation, resulting in inadequate blood oxygenation and hypoventilation.32,33 Atelectasis, hypoxemia, compromised CPR hemodynamics, and decreased cerebral oxygenation and perfusion are also possible if positive-pressure ventilation is not provided during CPR (eg, chest compressions-only CPR) or when ventilation rates are too low.34,35

View this table:
Table 2.

Summary of Outcomes From Included Human Studies on Ventilation and Oxygenation During Cardiopulmonary Resuscitation

View this table:
Table 3.

Summary of Outcomes From Included Randomized Experimental Animal Studies on Ventilation and Oxygenation During Cardiopulmonary Resuscitation

Conversely, several observational clinical studies have demonstrated that delivering high ventilation rates leading to hyperventilation is common during CPR in all settings.11,12,36-40 In 2004, Aufderheide et al11,12 conducted a clinical observation study and an experimental animal study to quantify excessive ventilation during out-of-hospital CPR in humans and its effects on coronary perfusion pressure and survival in pigs. The clinical study observed an average ventilation rate of 30 ± 3.2 breaths/min delivered during CPR on 13 adult subjects, none of whom survived.11,12 The animal study, which included 2 protocols involving a total of 30 pigs, found that a higher ventilation rate of 30 breaths/min was significantly associated with increased intrathoracic pressure (P < .001), decreased coronary perfusion pressure (P = .03), and reduced survival rates (P = .006).11,12 Other experimental animal studies have reported similar hemodynamic findings associated with higher ventilation rates.41-43 One study reported a significant association between the reduction of ventilation rates and a higher rate of ROSC.42 In contrast, 2 experimental animal studies have shown that a reduction in ventilation rates was not associated with an improved rate of ROSC, nor did the reduction demonstrate any improved hemodynamic effects during CPR.44,45 In 2 observational studies on human subjects, researchers found no significant differences in ventilation rates delivered during CPR between subjects who achieved ROSC and those who did not.38,39 In 2023, results from a randomized controlled trial (RCT) on subjects with CA indicated that a ventilation rate of 20 breaths/min versus 10 breaths/min during out-of-hospital CPR increased minute ventilation significantly; however, there was no significant difference in the CO2 washout, acidemia, oxygenation, or the rate of successful ROSC.46

Ventilation rate is not the only component of ventilation that clinicians need to consider. VT, inspiratory time, airway pressures, and the interaction between chest compressions and ventilation are also considerations.47 The current understanding of the interplay of these factors is limited, underscoring the need for further research.47 O’Neill and Deakin36 conducted one of the first human clinical studies reporting ventilation variables delivered during adult CPR, which included VT. They reported a median delivered VT of 618.5 mL with volumes ranging from 374–923 mL. They also reported median peak inspiratory pressures of 60.6 cm H2O, ranging from 46–106 cm H2O.36 The authors concluded that hyperventilation was common but more from a high ventilation rate than a high VT.36

As stated previously, the current recommended VT during CPR is 500–600 mL. The rationale behind this recommendation in CPR guidelines is that ventilation in this range is usually appropriate to produce visible chest rise and maintain gas exchange in apneic patients in CA. These volumes also help to avoid excessive airway pressures and gastric overdistention.48-50 It is notable that the current recommendations are supported by RCTs conducted more than 20 years ago, and no evidence since then has been able to convincingly refute these VT targets.49,50 The current VT recommendations are also supported by physiological models of respiratory gas exchange that have shown that VT of 600 mL via BMV was enough to maintain appropriate gas exchange when ventilation rates were maintained at 12 breaths/min.51 Notably; however, Ruemmler et al52 used an experimental animal study to demonstrate that ultralow VT (2–4 mL/kg) during resuscitation promotes lung protection and positive neurological outcomes due to decreased inflammation.52 At present, the optimal ventilation rate and VT that contribute to favorable outcomes such as ROSC, meaningful neurological recovery, and survival across diverse patient populations remain unknown. To address this critical gap, further research, particularly through large-scale human clinical trials, is necessary.

Oxygen: How Much?

A critical consideration in CPR is whether ventilation with 100% oxygen, as opposed to lower oxygen concentrations, is necessary. During CA, the body experiences a state of low blood flow, significantly reducing oxygen delivery to tissues and depleting intracellular oxygen reserves.53 High oxygen concentrations (eg, 100% oxygen) during CPR are thought to be needed to restore intracellular oxygen levels and avoid hypoxia and its detrimental impacts on outcomes. In a low-flow state, it is unlikely that oxygen delivery will exceed demand or that elevated PaO2 will result in hyperoxia, which theoretically underlies the increased oxidative injury observed during reperfusion.10,53 However, after the restoration of blood flow and adequate oxygen delivery to tissues, high oxygen concentrations may lead to hyperoxia, which is thought to be harmful.53 For example, a retrospective observational study by Kilgannon et al54 showed that post-ROSC hyperoxia was significantly associated with higher in-hospital mortality rates.54

Two observational studies assessing PaO2 during OHCA showed that a high PaO2 during CPR (due to high concentrations of oxygen being delivered during CPR) was associated with improved survival rates to hospital admission.55,56 Interestingly, the harmful effects of hyperoxia post ROSC do not appear to be an issue for high PaO2 values measured during CPR (see Tables 2 and 3), suggesting that providing the highest oxygen concentration possible during CPR is safe and effective.55,56 However, questions remain regarding how high of an oxygen concentration is actually needed. For example, in an animal study, 50% oxygen delivered during CPR was compared to 100% oxygen.57 The authors reported no significant differences in clinical outcomes, such as ROSC and time to ROSC; however, the administration of 50% oxygen did not alleviate the disturbances in mitochondrial respiration.57 At present, CPR guidelines suggest that clinicians administer the highest possible oxygen concentration during CPR when supplemental oxygen is available.10,20,21 It appears that the harmful effects of hyperoxia are not as profound during the low-flow state of CPR. In the early post-CA period, guidelines suggest that it is reasonable to provide the highest oxygen percent available until oxyhemoglobin saturations can be measured. Further prospective clinical studies are needed to determine whether an optimal oxygenation level exists during CPR and, if so, how clinicians can monitor oxygen in real-time to make necessary adjustments to improve outcomes.10,20,21

Monitoring Quality and Effectiveness

Capnography.

Capnography during CPR provides critical feedback on the quality of chest compressions, ventilation, and endotracheal tube placement.20,21,30,31 Guidelines suggest that low or decreasing end-tidal CO2 (PETCO2) levels may indicate the need to reassess CPR quality.21 They suggest that a PETCO2 value of more than 10 mm Hg or a sudden and sustained increase after intubation or 20 min of CPR may predict ROSC.20,21,30,31 They also suggest that PETCO2 values of 10–20 mm Hg during CPR may predict an increased chance of survival to discharge (see Table 1).20,21,30,31 However, guidelines do not recommend using PETCO2 values alone to make decisions regarding the continuation or termination of resuscitative efforts or to predict mortality.20,21,30,31 Studies have reported that the sensitivity and specificity of PETCO2 for detecting ROSC varies, and in fact, the PETCO2 values associated with ROSC detection remain unclear.58-60 For example, a retrospective case-control study of 108 OHCA subjects reported an abrupt increase in PETCO2 (≥ 10 mm Hg) had an 80% sensitivity and 41% specificity for detecting ROSC.59 Whereas, Lui et al,60 in a cross-sectional study of 178 OHCA subjects, reported that a rise in PETCO2 value (≥ 10 mm Hg) had 33% sensitivity and 97% specificity for detecting ROSC.

When utilizing waveform capnography during CPR to monitor ventilation rates and quality, clinicians must consider other confounding factors that may impact its applicability.57 Artifacts caused by chest compressions and the impact of certain drugs, such as sodium bicarbonate or adrenaline, as well as chest compression quality and ventilation pattern variations, may affect capnography and PETCO2.values.58 PETCO2 is recognized as an indicator of cardiac output in low-flow states. During CA, the body is in a low-flow state, limiting pulmonary circulation and compromising gas exchange, resulting in limited CO2 clearance and low PETCO2.61 With high-quality chest compressions during CPR, blood flow and gas exchange are improved, and PETCO2 increases.61 In a multi-center cohort study that assessed 583 OHCA and IHCA subjects, a significant association was found between higher PETCO2 values and increased chest compression depth, as well as a significant correlation between higher ventilation rates and lower PETCO2.values.61 Leturiondo et al62 showed that the presence of chest compression artifacts decreased sensitivity and positive predictive value of waveform capnography to well below 80%, in addition to a 50% reported error in the ventilation rate measurement.62 Given the perceived importance of PETCO2 monitoring, efforts are being directed toward developing innovative techniques and algorithms capable of delivering more accurate, real-time ventilation feedback.63,64 Two experimental studies of automated algorithms incorporated with capnography have improved the overall sensitivity and positive predictive value for detecting ventilation rates during chest compression.63,64 Hopefully, these algorithms or others can provide valuable information that will improve the capabilities of capnography.

A knowledge gap exists regarding the use of capnography during CPR, including confounding factors, clinical applicability, and prognostic values.20 Specifically, the impact of CA etiology, chest compressions, and ventilation rates on capnography values during CPR is not fully understood.20 Cutoff values for predicting short- or long-term outcomes after CA have not been established.20 Despite practical limitations and the multiple confounding factors that limit capnography’s applicability, it is commonly used during CPR.65 Clinicians need to be aware of the current limitations of the technology; thus, clinical education initiatives should focus on the capabilities and limitations of capnography in an effort to optimize its use during CPR. More research and a clearer understanding of its use are needed to optimize this technology.

Real-time ventilation feedback systems/devices.

In practice, ventilation during CPR is provided without feedback, and clinicians often rely on their perception of adequacy based on visual observation on chest rise. In a 2019 survey of Canadian emergency medical physicians, only 12% utilized CPR feedback devices, whereas 41.2% relied only on visual observation to assess CPR quality.66 Studies continue to demonstrate that variables such as VT delivered during CPR are often not within the recommended ranges.67,68 In a cross-sectional study evaluating the delivery of VT and ventilation rates during simulated resuscitation, Scott et al68 found a significant variation in VT delivered by clinicians during manual ventilation. Fewer than half of the participants delivered VT within the recommended range of 5–8 mL/kg of predicted body weight (PBW) for the simulated subject. However, the participants could meet the target ventilation rate of 10 breaths/min.68 To improve CPR quality, guidelines suggest using feedback devices is reasonable.21,22,30

Commercially available ventilation feedback devices offer real-time guidance, monitoring, and corrective feedback on ventilation rates and volumes during CPR. Ventilation feedback device technology ranges from basic audiovisual ventilation rate timers to real-time feedback devices equipped with sensors that measure VT and ventilation rates during CPR.69,-,74 Modern devices are small, portable, easy to use, and connected between the resuscitation bag and ventilation interface.72-74 Simulation-based studies have shown that real-time ventilation feedback devices improve ventilation (eg, reducing hypoventilation and hyperventilation) delivery during CPR and increase adherence to CPR guidelines.69-74 Ongoing efforts are being made to improve these devices’ accuracy, usability, and integration. Innovations such as wireless connectivity for remote monitoring and data analysis, machine learning algorithms for improved decision support, and automated CPR devices that adjust ventilation based on physiological feedback have been described.69-74 However, whereas promising, there remains a lack of human clinical studies that have assessed the impact of utilizing these devices on patient outcomes.21,30

Mechanical Ventilation as an Alternative to Manual Ventilation During CPR

The use of mechanical ventilation, as an alternative to manual ventilation, during CPR has been proposed.75,76 In a 2018 international survey, 46% (223/490 respondents) reported using mechanical ventilators during CPR for intubated patients. Seventy-two percent of surveyed clinicians reported using volume controlled modes when using a mechanical ventilator.65 Sahu and colleagues75 proposed a “six-dial” strategy for using mechanical ventilation during CPR for patients who were already intubated. Their strategy includes using volume controlled ventilation with (1) PEEP of 0 cm H2O, (2) VT of 8 mL/kg with an FIO2 at 1.0, (3) ventilation rate of 10 breaths/min, (4) maximum peak inspiratory pressure alarm of 60 cm H2O, (5) switching OFF of the trigger sensitivity, and (6) inspiratory-to-expiratory-time ratio (I-E) of 1:5.75 This proposed strategy was based on clinical application experience in one hospital emergency department and settings similar to established CPR guidelines.75 However, it is important to note that this method has not been evaluated in large clinical trials to establish its safety and effectiveness.75 In 2023, an RCT (CPR-VENT) compared the efficacy of mechanical ventilation to BMV ventilation during CPR in subjects in emergency departments.76 Sixty CA adult subjects receiving CPR were randomized into 2 groups, 30 subjects in each.76 The control group received BMV during CPR, whereas the intervention (mechanical ventilation) group received ventilation via a Hamilton-C1 ventilator (version SW 2.2.x, Hamilton Medical, Bonaduz, Switzerland) right after intubation.76 The ventilator was set on volume control, with a VT of 6–7 mL/kg, ventilation rate 10 breaths/min, PEEP 0 cm H2O, inspiratory time of 1 s, I:E ratio of 1:5, and FIO2 of 1.0. For subjects with unknown ideal body weights, the VT was set at 500 mL for males and 400 mL for females.76 Ventilation parameters in this RCT were similar to the ventilation strategy Sahu and colleagues proposed and recommended ventilation values by CPR guidelines.75,76 The result showed no significant difference in PaO2 values between the control group (36.5 mm Hg, interquartile range [IQR] 14–70 mm Hg) and the intervention group (29 mm Hg, IQR 15–70 mm Hg, P = .88).76 The resuscitation outcomes and complications of subjects between the control and intervention groups were not significantly different, ROSC (13, 43% vs 15, 50%, respectively, P = .80), survival to hospital admission (10, 33% vs 11, 37%, respectively, P > .99), survival to hospital discharge (3, 10% vs 5, 17%, respectively, P = .71), survival with good neurological outcome (0 vs 2, 7%, respectively, P = .49), and pneumothorax was not observed even though not all subjects received chest radiography.76 Whereas no differences in outcomes were noted, this RCT did demonstrate the feasibility and safety of mechanical ventilation during CPR in intubated subjects with CA.76

Currently, it is unclear if using a mechanical ventilator offers any real advantage over manual ventilation during CPR. Whereas it appears safe, the optimal mechanical ventilation strategy during CPR is not yet known, and further research is needed.

Ventilation and Oxygenation Post–Cardiac Arrest

Ventilation and oxygenation, if not managed carefully post CA, may lead to detrimental pathophysiological consequences. After CA, the body may undergo a systemic inflammatory state known as post-CA syndrome.77 The syndrome is characterized by 4 primary components: brain injury, myocardial dysfunction, systemic response to ischemia/reperfusion, and persistent precipitating pathology.77,78 The main pathophysiological features of post-CA syndrome involve oxidative stress, coagulation abnormalities, and extensive inflammation, all contributing to multi-organ failure.77,79

Hyperventilation may lead to cerebral vasoconstriction and secondary ischemic brain injury, especially during the early stage after ROSC, due to cerebral vasculature sensitivity to PaCO2 and impaired cerebral autoregulation. Hypoventilation may result in cerebral vasodilation, increasing blood flow to the brain, which could result in cerebral edema and reperfusion injury.77,-,81 Prolonged administration of high FIO2 may lead to hyperoxia, resulting in increased reactive oxygen species production, worsened oxidative stress, mitochondrial dysfunction, neuronal injury, and organ failure.77,78,82,-,84 Hypoxia may worsen the existing ischemic injury, permanent cellular injury, and organ dysfunction.77,78,82-84

ARDS is common in patients post CA.78,85,86 Two clinical studies reported that 48–72% of intubated post-CA subjects developed ARDS within 24–48 h after ROSC, which is associated with increased mortality.85,86 Thus, several recommendations have been made regarding the pulmonary management of patients who are post CA.

Recommended Clinical Management Strategies for Patients Post–Cardiac Arrest

Current recommendations for mechanical ventilation post CA include implementing a strategy aimed at lung protection and adequate gas exchange.21,58,78 In general, recommendations suggest that clinicians should target normal PaO2 and PaCO2 while avoiding hyperoxia and hypercarbia.21,58,78 A lung-protective strategy in intubated patients post CA is particularly important given the high incidence of ARDS post CA.78,85,86 Lung-protective strategies include (1) VT of 4–8 mL/kg PBW, (2) plateau pressure < 30 cm H2O and driving pressure < 15 cm H2O, and (3) titrating PEEP and FIO2 to achieve normoxia.78 Recent observational studies associated targeting normocapnia for ventilated subjects post CA with better neurological outcomes.87,88 Some studies have reported an association between hypercarbia and poor neurological function and increased in-hospital mortality after OHCA.89,90 However, the evidence is somewhat conflicting. In 2023, an RCT (the TAME study) included 1,700 subjects from 63 ICUs in 17 countries, compared targeted mild hypercapnia (PaCO2 of 50–55 mm Hg) to normocapnia (PaCO2 of 35–45 mm Hg).91 The authors reported no significant differences between the mild hypercapnia group and the normocapnia group in terms of favorable neurological outcomes (43.5% vs 44.6%; relative risk 0.98 [95% CI 0.87–1.11], P = .76, respectively) and 6 months mortality (48.2% vs 45.9%; relative risk 1.05 [95% CI 0.94–1.16], respectively).91

As for oxygenation, AHA guidelines recommend titrating FIO2 to target SpO2 values of 92–98%.21 However, recommendations suggest that FIO2 should not be titrated post CA until a reliable assessment of blood oxygen saturation is available, such as pulse oximetry or arterial blood gases.21 A 2018 systematic review and meta-analysis assessed the effect of hyperoxia on mortality and reported an association between post-CA hyperoxia and higher mortality compared to normoxia (odds ratio 1.34 [95% CI 1.08–1.67], P = .008, respectively).18 In contrast, 3 RCTs, including the ICU-ROX study, reported no significant difference in neurological outcomes and mortality between liberal (hyperoxia) and conservative (normoxia) oxygen strategies.92,-,94 However, the sum of the evidence suggests that conservative oxygen management is the best for patients after ROSC.18,92-94

In 2022, Battaglini et al82 proposed 10 rules for optimizing mechanical ventilation and targets post CA. They suggest that protective and personalized mechanical ventilation is warranted even in patients without ARDS and after CA.82 For ventilation, they proposed VT of 6–8 mL/kg of PBW, ventilation frequency of 8–16 breaths/min, targeting PaCO2 of 35–50 mm Hg, maintaining plateau pressures ≤ 20 cm H2O, driving pressures < 13 cm H2O, and a mechanical power < 17 J/min.82 For oxygenation, they suggest PEEP ≥ 5 cm H2O and the titration of FIO2 to achieve normoxia (PaO2 values of 70–100 mm Hg).82 Whereas literature recommendations on ventilation and oxygenation post CA may vary slightly, it is generally agreed that clinicians should prioritize lung protection and aim for relatively normal targets for PaCO2 and PaO2.

Summary

Effective ventilation and oxygenation are critical components of CPR, requiring careful attention to technique and adherence to evidence-based guidelines. Excessive ventilation and inadequate ventilation may negatively impact patient outcomes. Similarly, hypoxia and hyperoxia can also lead to adverse outcomes, emphasizing the need for optimal oxygenation levels during and after CPR. Real-time feedback devices and mechanical ventilation show promise, but further research is needed to establish their efficacy. Post-CA care should focus on lung protection strategies to mitigate the risk of ARDS and other complications. Continuous clinical research, updates to guidelines, and training for health care providers are essential to improve patient outcomes in CPR.

Acknowledgments

OpenAI (2023). ChatGPT with GPT-4 architecture was used to generate some draft language to improve readability. The authors revised the language suggestions to their own liking and take responsibility for the content of this publication.

Footnotes

  • Correspondence: J Brady Scott PhD RRT RRT-ACCS AE-C FAARC, Department of Cardiopulmonary Sciences, Division of Respiratory Care, Rush University. 600 S. Paulina Street, Suite 751, Chicago, IL. 60612. E-mail: Jonathan_B_Scott{at}rush.edu

  • Dr Scott discloses relationships with the American Association for Respiratory Care (AARC) and Relias Media. Dr Li discloses relationships with AARC, Fisher & Paykel Healthcare, Aerogen, MEKICS Co, Vincent, the Rice Foundation, and Heyer. Dr Li is a section editor for Respiratory Care. Drs Scott and Li disclose patent applications on a device to monitor and alarm manual ventilation parameters during cardiopulmonary resuscitation (WO2021167870A1; US20230131417A1). Mr Algahtani has disclosed no conflicts of interest.

  • Dr Scott presented a version of this paper during the New Horizons Symposium at the AARC Congress 2023, held November 5– 8, 2023, in Nashville, Tennessee.

REFERENCES

  1. 1.↵
    1. Wong MK,
    2. Morrison LJ,
    3. Qiu F,
    4. Austin PC,
    5. Cheskes S,
    6. Dorian P,
    7. et al
    . Trends in short- and long-term survival among out-of-hospital cardiac arrest patients alive at hospital arrival. Circulation 2014;130(21):1883-1890.
    OpenUrlAbstract/FREE Full Text
  2. 2.↵
    1. Tsao CW,
    2. Aday AW,
    3. Almarzooq ZI,
    4. Alonso A,
    5. Beaton AZ,
    6. Bittencourt MS,
    7. et al
    . Heart disease and stroke statistics-2022 update: a report from the American Heart Association. Circulation 2022;145(8):e153-e639.
    OpenUrlCrossRefPubMed
  3. 3.↵
    1. Wyckoff MH,
    2. Greif R,
    3. Morley PT,
    4. Ng K-C,
    5. Olasveengen TM,
    6. Singletary EM,
    7. et al
    ; Collaborators. 2022 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations: summary from the basic life support; advanced life support; pediatric life support; neonatal life support; education, implementation, and teams; and first aid task forces. Resuscitation 2022;181:208-288.
    OpenUrlCrossRefPubMed
  4. 4.↵
    1. Hessulf F,
    2. Herlitz J,
    3. Rawshani A,
    4. Aune S,
    5. Israelsson J,
    6. Södersved-Källestedt M-L,
    7. et al
    . Adherence to guidelines is associated with improved survival following in-hospital cardiac arrest. Resuscitation 2020;155:13-21.
    OpenUrlPubMed
  5. 5.↵
    1. Girotra S,
    2. Nallamothu BK,
    3. Spertus JA,
    4. Li Y,
    5. Krumholz HM,
    6. Chan PS
    ; American Heart Association Get with the Guidelines–Resuscitation Investigators. Trends in survival after in-hospital cardiac arrest. N Engl J Med 2012;367(20):1912-1920.
    OpenUrlCrossRefPubMed
  6. 6.↵
    1. Hessulf F,
    2. Karlsson T,
    3. Lundgren P,
    4. Aune S,
    5. Strömsöe A,
    6. Södersved Källestedt M-L,
    7. et al
    . Factors of importance to 30-day survival after in-hospital cardiac arrest in Sweden – A population-based register study of more than 18,000 cases. Int J Cardiol 2018;255:237-242.
    OpenUrlCrossRefPubMed
  7. 7.↵
    1. Gazmuri RJ,
    2. Ayoub I
    . Ventilation during CPR: a challenge to guidelines and a call for research on lingering scientific gaps. Resuscitation 2023;187:109811.
    OpenUrlPubMed
  8. 8.↵
    1. Cordioli RL,
    2. Grieco DL,
    3. Charbonney E,
    4. Richard J-C,
    5. Savary D
    . New physiological insights in ventilation during cardiopulmonary resuscitation. Curr Opin Crit Care 2019;25(1):37-44.
    OpenUrlPubMed
  9. 9.↵
    1. Kleinman ME,
    2. Brennan EE,
    3. Goldberger ZD,
    4. Swor RA,
    5. Terry M,
    6. Bobrow BJ,
    7. et al
    . Part 5: adult basic life support and cardiopulmonary resuscitation quality: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular Care. Circulation 2015;132(18 Suppl 2):S414-S435.
    OpenUrlFREE Full Text
  10. 10.↵
    1. Link MS,
    2. Berkow LC,
    3. Kudenchuk PJ,
    4. Halperin HR,
    5. Hess EP,
    6. Moitra VK,
    7. et al
    . Part 7: adult advanced cardiovascular life support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2015;132(18 Suppl 2):S444-464.
    OpenUrlFREE Full Text
  11. 11.↵
    1. Aufderheide TP,
    2. Lurie KG
    . Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med 2004;32(9 Suppl):S345-351.
    OpenUrlCrossRefPubMed
  12. 12.↵
    1. Aufderheide TP,
    2. Sigurdsson G,
    3. Pirrallo RG,
    4. Yannopoulos D,
    5. McKnite S,
    6. von Briesen C,
    7. et al
    . Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109(16):1960-1965.
    OpenUrlAbstract/FREE Full Text
  13. 13.↵
    1. Neth MR,
    2. Idris A,
    3. McMullan J,
    4. Benoit JL,
    5. Daya MR
    . A review of ventilation in adult out‐of‐hospital cardiac arrest. J Am Coll Emerg Physicians Open 2020;1(3):190-201.
    OpenUrlPubMed
  14. 14.↵
    1. Wenzel V,
    2. Idris AH,
    3. Banner MJ,
    4. Kubilis PS,
    5. Williams JLJ
    . Influence of tidal volume on the distribution of gas between the lungs and stomach in the non-intubated patient receiving positive-pressure ventilation. Crit Care Med 1998;26(2):364-368.
    OpenUrlCrossRefPubMed
  15. 15.↵
    1. Naito H,
    2. Hanafusa H,
    3. Hongo T,
    4. Yumoto T,
    5. Yorifuji T,
    6. Weissman A,
    7. et al
    . Effect of stomach inflation during cardiopulmonary resuscitation on return of spontaneous circulation in out-of-hospital cardiac arrest patients: a retrospective observational study. Resuscitation 2023;193:109994.
    OpenUrlPubMed
  16. 16.↵
    1. Singer M,
    2. Young PJ,
    3. Laffey JG,
    4. Asfar P,
    5. Taccone FS,
    6. Skrifvars MB,
    7. et al
    . Dangers of hyperoxia. Crit Care 2021;25(1):440.
    OpenUrlCrossRefPubMed
  17. 17.↵
    1. Hochberg CH,
    2. Semler MW,
    3. Brower RG
    . Oxygen toxicity in critically ill adults. Am J Respir Crit Care Med 2021;204(6):632-641.
    OpenUrlPubMed
  18. 18.↵
    1. Patel JK,
    2. Kataya A,
    3. Parikh PB
    . Association between intra- and post-arrest hyperoxia on mortality in adults with cardiac arrest: a systematic review and meta-analysis. Resuscitation 2018;127:83-88.
    OpenUrlPubMed
  19. 19.↵
    1. Wang C-H,
    2. Chang W-T,
    3. Huang C-H,
    4. Tsai M-S,
    5. Yu P-H,
    6. Wang A-Y,
    7. et al
    . The effect of hyperoxia on survival following adult cardiac arrest: a systematic review and meta-analysis of observational studies. Resuscitation 2014;85(9):1142-1148.
    OpenUrlCrossRefPubMed
  20. 20.↵
    1. Callaway CW,
    2. Soar J,
    3. Aibiki M,
    4. Böttiger BW,
    5. Brooks SC,
    6. Deakin CD,
    7. et al
    ; Advanced Life Support Chapter Collaborators. Part 4: advanced life support: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2015;132(16 Suppl 1):S84-145.
    OpenUrlFREE Full Text
  21. 21.↵
    1. Panchal AR,
    2. Bartos JA,
    3. Cabañas JG,
    4. Donnino MW,
    5. Drennan IR,
    6. Hirsch KG,
    7. et al
    ; Adult Basic and Advanced Life Support Writing Group. Part 3: adult basic and advanced life support: 2020 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2020;142(16_suppl_2):S366-S468.
    OpenUrlCrossRefPubMed
  22. 22.↵
    1. Panchal AR,
    2. Berg KM,
    3. Hirsch KG,
    4. Kudenchuk PJ,
    5. Del Rios M,
    6. Cabañas JG,
    7. et al
    . 2019 American Heart Association focused update on advanced cardiovascular life support: use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resuscitation during cardiac arrest: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2019;140(24):e881-e894.
    OpenUrlPubMed
  23. 23.↵
    1. Travers AH,
    2. Perkins GD,
    3. Berg RA,
    4. Castren M,
    5. Considine J,
    6. Escalante R,
    7. et al
    ; Basic Life Support Chapter Collaborators. Part 3: adult basic life support and automated external defibrillation: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation 2015;95:e43-e69.
    OpenUrlCrossRefPubMed
  24. 24.↵
    1. Olasveengen TM,
    2. De Caen AR,
    3. Mancini ME,
    4. Maconochie IK,
    5. Aickin R,
    6. Atkins DL,
    7. et al
    ; ILCOR Collaborators. 2017 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations summary. Resuscitation 2017;121:201-214.
    OpenUrlCrossRefPubMed
  25. 25.↵
    1. Olasveengen TM,
    2. Mancini ME,
    3. Perkins GD,
    4. Avis S,
    5. Brooks S,
    6. Castrén M,
    7. et al
    ; Adult Basic Life Support Collaborators. Adult basic life support: 2020 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation 2020;156:A35-A79.
    OpenUrlPubMed
  26. 26.↵
    1. Soar J,
    2. Maconochie I,
    3. Wyckoff MH,
    4. Olasveengen TM,
    5. Singletary EM,
    6. Greif R,
    7. et al
    . 2019 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations: summary from the basic life support; advanced life support; pediatric life support; neonatal life support; education, implementation, and teams; and first aid task forces. Circulation 2019;140(24):e826-e880.
    OpenUrlPubMed
  27. 27.↵
    1. Wyckoff MH,
    2. Singletary EM,
    3. Soar J,
    4. Olasveengen TM,
    5. Greif R,
    6. Liley HG,
    7. et al
    . 2021 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations: summary from the basic life support; advanced life support; neonatal life support; education, implementation, and teams; first aid task forces; and the COVID-19 Working Group. Circulation 2022;145(9):e645-e721.
    OpenUrlPubMed
  28. 28.↵
    1. Nolan JP,
    2. Maconochie I,
    3. Soar J,
    4. Olasveengen TM,
    5. Greif R,
    6. Wyckoff MH,
    7. et al
    . Executive summary: 2020 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2020;142(16_suppl_1):S2-S27.
    OpenUrlPubMed
  29. 29.↵
    1. Berg KM,
    2. Bray JE,
    3. Ng K-C,
    4. Liley HG,
    5. Greif R,
    6. Carlson JN,
    7. et al
    ; Collaborators. 2023 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations: summary from the basic life support; advanced life support; pediatric life support; neonatal life support; education, implementation, and teams; and first aid task forces. Circulation 2023;148(24):e187-e280.
    OpenUrlPubMed
  30. 30.↵
    1. Berg KM,
    2. Soar J,
    3. Andersen LW,
    4. Böttiger BW,
    5. Cacciola S,
    6. Callaway CW,
    7. et al
    ; Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2020;142(16_suppl_1):S92-S139.
    OpenUrlPubMed
  31. 31.↵
    1. Soar J,
    2. Berg KM,
    3. Andersen LW,
    4. Böttiger BW,
    5. Cacciola S,
    6. Callaway CW,
    7. et al
    ; Adult Advanced Life Support Collaborators. Adult advanced life support: 2020 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation 2020;156:A80-A119.
    OpenUrlPubMed
  32. 32.↵
    1. Lurie KG,
    2. Nemergut EC,
    3. Yannopoulos D,
    4. Sweeney M
    . The physiology of cardiopulmonary resuscitation. Anesth Analg 2016;122(3):767-783.
    OpenUrlCrossRefPubMed
  33. 33.↵
    1. Yannopoulos D,
    2. Tang W,
    3. Roussos C,
    4. Aufderheide TP,
    5. Idris AH,
    6. Lurie KG
    . Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest. Respir Care 2005;50(5):628-635.
    OpenUrlAbstract/FREE Full Text
  34. 34.↵
    1. Markstaller K,
    2. Rudolph A,
    3. Karmrodt J,
    4. Gervais HW,
    5. Goetz R,
    6. Becher A,
    7. et al
    . Effect of chest compressions only during experimental basic life support on alveolar collapse and recruitment. Resuscitation 2008;79(1):125-132.
    OpenUrlPubMed
  35. 35.↵
    1. Lurie KG,
    2. Yannopoulos D,
    3. McKnite SH,
    4. Herman ML,
    5. Idris AH,
    6. Nadkarni VM,
    7. et al
    . Comparison of a 10-breaths-per-minute versus a 2-breaths-per-minute strategy during cardiopulmonary resuscitation in a porcine model of cardiac arrest. Respir Care 2008;53(7):862-870.
    OpenUrlAbstract/FREE Full Text
  36. 36.↵
    1. O’Neill JF,
    2. Deakin CD
    . Do we hyperventilate cardiac arrest patients? Resuscitation 2007;73(1):82-85.
    OpenUrlCrossRefPubMed
  37. 37.
    1. Maertens VL,
    2. De Smedt LEG,
    3. Lemoyne S,
    4. Huybrechts SAM,
    5. Wouters K,
    6. Kalmar AF,
    7. et al
    . Patients with cardiac arrest are ventilated two times faster than guidelines recommend: an observational prehospital study using tracheal pressure measurement. Resuscitation 2013;84(7):921-926.
    OpenUrlCrossRefPubMed
  38. 38.↵
    1. Vissers G,
    2. Duchatelet C,
    3. Huybrechts SA,
    4. Wouters K,
    5. Hachimi-Idrissi S,
    6. Monsieurs KG
    . The effect of ventilation rate on outcome in adults receiving cardiopulmonary resuscitation. Resuscitation 2019;138:243-249.
    OpenUrlPubMed
  39. 39.↵
    1. Abella BS,
    2. Alvarado JP,
    3. Myklebust H,
    4. Edelson DP,
    5. Barry A,
    6. O’Hearn N,
    7. et al
    . Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA 2005;293(3):305-310.
    OpenUrlCrossRefPubMed
  40. 40.↵
    1. Abella BS,
    2. Edelson DP,
    3. Kim S,
    4. Retzer E,
    5. Myklebust H,
    6. Barry AM,
    7. et al
    . CPR quality improvement during in-hospital cardiac arrest using a real-time audiovisual feedback system. Resuscitation 2007;73(1):54-61.
    OpenUrlCrossRefPubMed
  41. 41.↵
    1. Yannopoulos D,
    2. Sigurdsson G,
    3. McKnite S,
    4. Benditt D,
    5. Lurie KG
    . Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest. Resuscitation 2004;61(1):75-82.
    OpenUrlCrossRefPubMed
  42. 42.↵
    1. Yannopoulos D,
    2. Aufderheide TP,
    3. Gabrielli A,
    4. Beiser DG,
    5. McKnite SH,
    6. Pirrallo RG,
    7. et al
    . Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med 2006;34(5):1444-1449.
    OpenUrlCrossRefPubMed
  43. 43.↵
    1. Hayes MM,
    2. Ewy GA,
    3. Anavy ND,
    4. Hilwig RW,
    5. Sanders AB,
    6. Berg RA,
    7. et al
    . Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out-of-hospital ventricular fibrillation. Resuscitation 2007;74(2):357-365.
    OpenUrlCrossRefPubMed
  44. 44.↵
    1. Hwang SO,
    2. Kim SH,
    3. Kim H,
    4. Jang YS,
    5. Zhao PG,
    6. Lee KH,
    7. et al
    . Comparison of 15:1, 15:2, and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation in a canine model of a simulated, witnessed cardiac arrest. Acad Emerg Med 2008;15(2):183-189.
    OpenUrlCrossRefPubMed
  45. 45.↵
    1. Gazmuri RJ,
    2. Ayoub IM,
    3. Radhakrishnan J,
    4. Motl J,
    5. Upadhyaya MP
    . Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO2. Resuscitation 2012;83(2):259-264.
    OpenUrlCrossRefPubMed
  46. 46.↵
    1. Prause G,
    2. Zoidl P,
    3. Eichinger M,
    4. Eichlseder M,
    5. Orlob S,
    6. Ruhdorfer F,
    7. et al
    . Mechanical ventilation with 10 versus 20 breaths per minute during cardiopulmonary resuscitation for out-of-hospital cardiac arrest: a randomized controlled trial. Resuscitation 2023;187:109765.
    OpenUrlPubMed
  47. 47.↵
    1. Vissers G,
    2. Soar J,
    3. Monsieurs KG
    . Ventilation rate in adults with a tracheal tube during cardiopulmonary resuscitation: a systematic review. Resuscitation 2017;119:5-12.
    OpenUrlPubMed
  48. 48.↵
    1. Berg RA,
    2. Hemphill R,
    3. Abella BS,
    4. Aufderheide TP,
    5. Cave DM,
    6. Hazinski MF,
    7. et al
    . Part 5: adult basic life support. Circulation 2010;122(18 Suppl 3):S685-S705.
    OpenUrlFREE Full Text
  49. 49.↵
    1. Wenzel V,
    2. Keller C,
    3. Idris AH,
    4. Dörges V,
    5. Lindner KH,
    6. Brimacombe JR
    . Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk? Resuscitation 1999;43(1):25-29.
    OpenUrlCrossRefPubMed
  50. 50.↵
    1. Dörges V,
    2. Ocker H,
    3. Hagelberg S,
    4. Wenzel V,
    5. Schmucker P
    . Optimization of tidal volumes given with self-inflatable bags without additional oxygen. Resuscitation 2000;43(3):195-199.
    OpenUrlCrossRefPubMed
  51. 51.↵
    1. Fitz-Clarke JR
    . Effect of tidal volume on gas exchange during rescue ventilation. Respir Physiol Neurobiol 2020;273:103335.
    OpenUrlPubMed
  52. 52.↵
    1. Ruemmler R,
    2. Ziebart A,
    3. Moellmann C,
    4. Garcia-Bardon A,
    5. Kamuf J,
    6. Kuropka F,
    7. et al
    . Ultralow tidal volume ventilation-A novel and effective ventilation strategy during experimental cardiopulmonary resuscitation. Resuscitation 2018;132:56-62.
    OpenUrlPubMed
  53. 53.↵
    1. Neumar RW
    . Optimal oxygenation during and after cardiopulmonary resuscitation. Curr Opin Crit Care 2011;17(3):236-240.
    OpenUrlCrossRefPubMed
  54. 54.↵
    1. Kilgannon JH,
    2. Jones AE,
    3. Shapiro NI,
    4. Angelos MG,
    5. Milcarek B,
    6. Hunter K,
    7. et al
    ; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA 2010;303(21):2165-2171.
    OpenUrlCrossRefPubMed
  55. 55.↵
    1. Spindelboeck W,
    2. Schindler O,
    3. Moser A,
    4. Hausler F,
    5. Wallner S,
    6. Strasser C,
    7. et al
    . Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission. Resuscitation 2013;84(6):770-775.
    OpenUrlCrossRefPubMed
  56. 56.↵
    1. Spindelboeck W,
    2. Gemes G,
    3. Strasser C,
    4. Toescher K,
    5. Kores B,
    6. Metnitz P,
    7. et al
    . Arterial blood gases during and their dynamic changes after cardiopulmonary resuscitation: a prospective clinical study. Resuscitation 2016;106:24-29.
    OpenUrlPubMed
  57. 57.↵
    1. Nelskylä A,
    2. Nurmi J,
    3. Jousi M,
    4. Schramko A,
    5. Mervaala E,
    6. Ristagno G,
    7. et al
    . The effect of 50% compared to 100% inspired oxygen fraction on brain oxygenation and post–cardiac arrest mitochondrial function in experimental cardiac arrest. Resuscitation 2017;116:1-7.
    OpenUrlPubMed
  58. 58.↵
    1. Sandroni C,
    2. De Santis P,
    3. D’Arrigo S
    . Capnography during cardiac arrest. Resuscitation 2018;132:73-77.
    OpenUrlPubMed
  59. 59.↵
    1. Pokorná M,
    2. Necas E,
    3. Kratochvíl J,
    4. Skripský R,
    5. Andrlík M,
    6. Franek O
    . A sudden increase in partial pressure end-tidal carbon dioxide (PETCO2) at the moment of return of spontaneous circulation. J Emerg Med 2010;38(5):614-621.
    OpenUrlCrossRefPubMed
  60. 60.↵
    1. Lui CT,
    2. Poon KM,
    3. Tsui KL
    . Abrupt rise of end-tidal carbon dioxide level was a specific but nonsensitive marker of return of spontaneous circulation in patient with out-of-hospital cardiac arrest. Resuscitation 2016;104:53-58.
    OpenUrlPubMed
  61. 61.↵
    1. Sheak KR,
    2. Wiebe DJ,
    3. Leary M,
    4. Babaeizadeh S,
    5. Yuen TC,
    6. Zive D,
    7. et al
    . Quantitative relationship between end-tidal carbon dioxide and CPR quality during both in-hospital and out-of-hospital cardiac arrest. Resuscitation 2015;89:149-154.
    OpenUrlCrossRefPubMed
  62. 62.↵
    1. Leturiondo M,
    2. Gauna S. D,
    3. Ruiz JM,
    4. Gutiérrez JJ,
    5. Leturiondo LA,
    6. González-Otero DM,
    7. et al
    . Influence of chest compression artefact on capnogram-based ventilation detection during out-of-hospital cardiopulmonary resuscitation. Resuscitation 2018;124:63-68.
    OpenUrlPubMed
  63. 63.↵
    1. Aramendi E,
    2. Elola A,
    3. Alonso E,
    4. Irusta U,
    5. Daya M,
    6. Russell JK,
    7. et al
    . Feasibility of the capnogram to monitor ventilation rate during cardiopulmonary resuscitation. Resuscitation 2017;110:162-168.
    OpenUrlPubMed
  64. 64.↵
    1. Leturiondo M,
    2. Julio Gutierrez J,
    3. Ruiz De Gauna S,
    4. Ruiz J,
    5. Alberto Leturiondo L,
    6. Knox Russell J,
    7. et al
    . A method to suppress chest compression artifact enhancing capnography-based ventilation guidance during cardiopulmonary resuscitation. Computing in Cardiology 2018(45).
  65. 65.↵
    1. Cordioli RL,
    2. Brochard L,
    3. Suppan L,
    4. Lyazidi A,
    5. Templier F,
    6. Khoury A,
    7. et al
    . How ventilation is delivered during cardiopulmonary resuscitation: an international survey. Respir Care 2018;63(10):1293-1301.
    OpenUrlAbstract/FREE Full Text
  66. 66.↵
    1. Wright N,
    2. Lin Y,
    3. Cheng A
    . How is quality of cardiopulmonary resuscitation being assessed? A national survey of Canadian emergency medicine physicians. CJEM 2019;21(6):744-748.
    OpenUrlPubMed
  67. 67.↵
    1. Neth MR,
    2. Benoit JL,
    3. Stolz U,
    4. McMullan J
    . Ventilation in simulated out-of-hospital cardiac arrest resuscitation rarely meets guidelines. Prehosp Emerg Care 2021;25(5):712-720.
    OpenUrlPubMed
  68. 68.↵
    1. Scott JB,
    2. Schneider JM,
    3. Schneider K,
    4. Li J
    . An evaluation of manual tidal volume and respiratory rate delivery during simulated resuscitation. Am J Emerg Med 2021;45:446-450.
    OpenUrlPubMed
  69. 69.↵
    1. Charlton K,
    2. McClelland G,
    3. Millican K,
    4. Haworth D,
    5. Aitken-Fell P,
    6. Norton M
    . The impact of introducing real-time feedback on ventilation rate and tidal volume by ambulance clinicians in the northeast in cardiac arrest simulations. Resusc Plus 2021;6:100130.
    OpenUrlPubMed
  70. 70.↵
    1. Jones B,
    2. Aiello S,
    3. Govender K,
    4. Shaw B,
    5. Tseng B,
    6. Dawad Z,
    7. et al
    . The impact of a ventilation timing light on CPR Quality: a randomized crossover study. Resusc Plus 2023;14:100404.
    OpenUrlPubMed
  71. 71.↵
    1. You KM,
    2. Lee C,
    3. Kwon WY,
    4. Lee JC,
    5. Suh GJ,
    6. Kim KS,
    7. et al
    . Real-time tidal volume feedback guides optimal ventilation during simulated CPR. Am J Emerg Med 2017;35(2):292-298.
    OpenUrlPubMed
  72. 72.↵
    1. Kim JW,
    2. Park SO,
    3. Lee KR,
    4. Hong DY,
    5. Baek KJ
    . Efficacy of Amflow, a real-time-portable feedback device for delivering appropriate ventilation in critically ill patients: a randomized controlled, crossover simulation study. Emerg Med Int 2020;2020:e5296519.
    OpenUrl
  73. 73.↵
    1. Lyngby RM,
    2. Clark L,
    3. Kjoelbye JS,
    4. Oelrich RM,
    5. Silver A,
    6. Christensen HC,
    7. et al
    . Higher resuscitation guideline adherence in paramedics with use of real-time ventilation feedback during simulated out-of-hospital cardiac arrest: a randomized controlled trial. Resusc Plus 2021;5:100082.
    OpenUrlPubMed
  74. 74.↵
    1. Khoury A,
    2. De Luca A,
    3. Sall FS,
    4. Pazart L,
    5. Capellier G
    . Ventilation feedback device for manual ventilation in simulated respiratory arrest: a crossover manikin study. Scand J Trauma Resusc Emerg Med 2019;27(1):93.
    OpenUrlPubMed
  75. 75.↵
    1. Sahu AK,
    2. Timilsina G,
    3. Mathew R,
    4. Jamshed N,
    5. Aggarwal P
    . “Six-dial Strategy”–mechanical ventilation during cardiopulmonary resuscitation. Indian J Crit Care Med 2020;24(6):487-489.
    OpenUrlPubMed
  76. 76.↵
    1. Tangpaisarn T,
    2. Tosibphanom J,
    3. Sata R,
    4. Kotruchin P,
    5. Drumheller B,
    6. Phungoen P
    . The effects of mechanical versus bag-valve ventilation on gas exchange during cardiopulmonary resuscitation in emergency department patients: a randomized controlled trial (CPR-VENT). Resuscitation 2023;193:109966.
    OpenUrlPubMed
  77. 77.↵
    1. Neumar RW,
    2. Nolan JP,
    3. Adrie C,
    4. Aibiki M,
    5. Berg RA,
    6. Böttiger BW,
    7. et al
    . Post–cardiac arrest syndrome. Circulation 2008;118(23):2452-2483.
    OpenUrlFREE Full Text
  78. 78.↵
    1. Hirsch KG,
    2. Abella BS,
    3. Amorim E,
    4. Bader MK,
    5. Barletta JF,
    6. Berg K,
    7. et al
    ; American Heart Association and Neurocritical Care Society. Critical care management of patients after cardiac arrest: a scientific statement from the American Heart Association and Neurocritical Care Society. Circulation 2024;149(2):e168-e200.
    OpenUrlPubMed
  79. 79.↵
    1. Johnson NJ,
    2. Carlbom DJ,
    3. Gaieski DF
    . Ventilator management and respiratory care after cardiac arrest: oxygenation, ventilation, infection, and injury. Chest 2018;153(6):1466-1477.
    OpenUrlPubMed
  80. 80.↵
    1. Buunk G,
    2. van der Hoeven JG,
    3. Meinders AE,
    4. Frölich M
    . Cerebral vasoconstriction in comatose patients resuscitated from a cardiac arrest? Intensive Care Med 1996;22(11):1191-1196.
    OpenUrlCrossRefPubMed
  81. 81.↵
    1. Sundgreen C,
    2. Larsen FS,
    3. Herzog TM,
    4. Knudsen GM,
    5. Boesgaard S,
    6. Aldershvile J
    . Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest. Stroke 2001;32(1):128-132.
    OpenUrlAbstract/FREE Full Text
  82. 82.↵
    1. Battaglini D,
    2. Pelosi P,
    3. Robba C
    . Ten rules for optimizing ventilatory settings and targets in post–cardiac arrest patients. Crit Care 2022;26(1):390.
    OpenUrlPubMed
  83. 83.↵
    1. Vereczki V,
    2. Martin E,
    3. Rosenthal RE,
    4. Hof PR,
    5. Hoffman GE,
    6. Fiskum G
    . Normoxic resuscitation after cardiac arrest protects against hippocampal oxidative stress, metabolic dysfunction, and neuronal death. J Cereb Blood Flow Metab 2006;26(6):821-835.
    OpenUrlCrossRefPubMed
  84. 84.↵
    1. Nolan JP,
    2. Soar J,
    3. Cariou A,
    4. Cronberg T,
    5. Moulaert VRM,
    6. Deakin CD,
    7. et al
    ; European Society of Intensive Care Medicine. European Resuscitation Council and European Society of Intensive Care Medicine 2015 guidelines for post–resuscitation care. Intensive Care Med 2015;41(12):2039-2056.
    OpenUrlPubMed
  85. 85.↵
    1. Johnson NJ,
    2. Caldwell E,
    3. Carlbom DJ,
    4. Gaieski DF,
    5. Prekker ME,
    6. Rea TD,
    7. et al
    . The acute respiratory distress syndrome after out-of-hospital cardiac arrest: incidence, risk factors, and outcomes. Resuscitation 2019;135:37-44.
    OpenUrlCrossRefPubMed
  86. 86.↵
    1. Shih JA,
    2. Robertson HK,
    3. Issa MS,
    4. Grossestreuer AV,
    5. Donnino MW,
    6. Berg KM,
    7. et al
    . Acute respiratory distress syndrome after in-hospital cardiac arrest. Resuscitation 2022;177:78-84.
    OpenUrlPubMed
  87. 87.↵
    1. Hope Kilgannon J,
    2. Hunter BR,
    3. Puskarich MA,
    4. Shea L,
    5. Fuller BM,
    6. Jones C,
    7. et al
    . Partial pressure of arterial carbon dioxide after resuscitation from cardiac arrest and neurological outcome: a prospective multi-center protocol-directed cohort study. Resuscitation 2019;135:212-220.
    OpenUrlPubMed
  88. 88.↵
    1. Vaahersalo J,
    2. Bendel S,
    3. Reinikainen M,
    4. Kurola J,
    5. Tiainen M,
    6. Raj R,
    7. et al
    ; FINNRESUSCI Study Group. Arterial blood gas tensions after resuscitation from out-of-hospital cardiac arrest: associations with long-term neurologic outcome. Crit Care Med 2014;42(6):1463-1470.
    OpenUrlCrossRefPubMed
  89. 89.↵
    1. Wang HE,
    2. Prince DK,
    3. Drennan IR,
    4. Grunau B,
    5. Carlbom DJ,
    6. Johnson N,
    7. et al
    ; Resuscitation Outcomes Consortium (ROC) Investigators. Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest. Resuscitation 2017;120:113-118.
    OpenUrlPubMed
  90. 90.↵
    1. Roberts BW,
    2. Kilgannon JH,
    3. Chansky ME,
    4. Mittal N,
    5. Wooden J,
    6. Trzeciak S
    . Association between post-resuscitation partial pressure of arterial carbon dioxide and neurological outcome in patients with post–cardiac arrest syndrome. Circulation 2013;127(21):2107-2113.
    OpenUrlAbstract/FREE Full Text
  91. 91.↵
    1. Eastwood G,
    2. Nichol AD,
    3. Hodgson C,
    4. Parke RL,
    5. McGuinness S,
    6. Nielsen N,
    7. et al
    ; TAME Study Investigators. Mild hypercapnia or normocapnia after out-of-hospital cardiac arrest. N Engl J Med 2023;389(1):45-57.
    OpenUrlPubMed
  92. 92.↵
    1. Jakkula P,
    2. Reinikainen M,
    3. Hästbacka J,
    4. Loisa P,
    5. Tiainen M,
    6. Pettilä V,
    7. et al
    ; COMACARE study group. Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomized pilot trial. Intensive Care Med 2018;44(12):2112-2121.
    OpenUrlPubMed
  93. 93.↵
    1. Schmidt H,
    2. Kjaergaard J,
    3. Hassager C,
    4. Mølstrøm S,
    5. Grand J,
    6. Borregaard B,
    7. et al
    . Oxygen targets in comatose survivors of cardiac arrest. N Engl J Med 2022;387(16):1467-1476.
    OpenUrlCrossRefPubMed
  94. 94.↵
    The ICU-ROX Investigators and the Australian and New Zealand Intensive Care Society Clinical Trials Group. Conservative oxygen therapy during mechanical ventilation in the ICU. N Engl J Med 2020;382(11):989-998.
    OpenUrlCrossRefPubMed
Back to top

In this issue

 

Print
Download PDF
Article Alerts
Email Article
Citation Tools

Jump to section

Related Articles

Cited By...

Keywords