Conflict of Interest Declaration
The ILCOR Continuous Evidence Evaluation process is guided by a rigorous ILCOR Conflict of Interest policy. The following Task Force members and other authors were recused from the discussion as they declared a conflict of interest: N/A
The following Task Force members and other authors declared an intellectual conflict of interest and this was acknowledged and managed by the Task Force Chairs and Conflict of Interest committees: N/A
Task Force Synthesis Citation
Smith CM, Clancy C, Laslett S, Ong G, Thiagarajan R, Cash R, Considine J, Dainty K, Nehme Z, Samantaray A, Scholefield BR, Morrison LJ, Smyth M, Bray JE, on behalf of the International Liaison Committee on Resuscitation Basic Life Support and Pediatric Life Support Task Forces. Defining chest compression components – rate, depth, recoil based on clinical outcomes: a Scoping Review. [Internet] International Liaison Committee on Resuscitation (ILCOR) Basic Life Support Task Force and Pediatric Life Support Task Force, January 3, 2025. Available from: http://ilcor.org
Methodological Preamble and Link to Published Scoping Review
The continuous evidence evaluation process started with a scoping review of basic life support conducted by the ILCOR BLS Task Force Scoping Review team, with support from the Pediatric Life Support Task Force. Evidence for adult and pediatric literature was sought and considered by the Basic Life Support Adult Task Force and the Pediatric Task Force groups respectively.
A previous version of this scoping review was published in 2020 1.
Smith CM, Clancy C, Laslett S, Ong G, Thiagarajan R, Cash R, Considine J, Dainty K, Nehme Z, Samantaray A, Scholefield BR, Morrison LJ, Smyth M, Bray JE, on behalf of the International Liaison Committee on Resuscitation Basic Life Support and Pediatric Life Support Task Forces. Defining chest compression components – rate, depth, recoil based on clinical outcomes: a Scoping Review. Resus Plus [in draft]
PICOST
The PICOST (Population, Intervention, Comparator, Outcome, Study Designs and Timeframe)
Population: Adults, children and infants (excluding newborns) in any setting (in-hospital or out-of-hospital) with cardiac arrest
Intervention: Alternative chest compression rate, depth or chest wall recoil during cardiopulmonary resuscitation (CPR)
Comparators: Standard chest compression rate, depth or chest wall recoil during cardiopulmonary resuscitation (CPR)
Outcomes: Any clinical outcome for adults, children and infants (excluding newborns) – including survival with favorable neurological outcome (critical), survival to hospital discharge or 30 days (critical), return of spontaneous circulation (ROSC) (important); any physiological outcome – including blood pressure, end-tidal CO2 (including clinical outcomes as defined in the Pediatric Core Outcome Set for Cardiac Arrest for children 2).
Study Designs: Randomized controlled trials (RCTs) and non-randomized studies (non-randomized controlled trials, interrupted time series, controlled before-and-after studies, cohort studies) are eligible for inclusion.
Included studies can report on only one chest compression component or two or more components or the interaction between two or more components. Included studies must report a comparison between two or more chest compression rates and/or chest compression depths and/or measures of chest wall recoil and/or measures of chest wall leaning.
Timeframe: All years
Search Strategies
Literature search was last performed on 5th August 2025. Searches were performed in MEDLINE, Embase and Cochrane Library.
After removal of 5659 duplicates, we screened 16901 titles/abstracts in Covidence. 145 were taken forward for full-text review, where a further 107 articles were excluded. One article was identified from additional sources 3.
Key terms included the keywords compression*, depth*, lean*, recoil* and the MeSH terms ‘Heart Arrest’ and ‘Resuscitation’.
Inclusion and Exclusion criteria
Included studies could report on a single chest compression component (rate, depth or recoil/leaning), two or more components or the interaction between two or more components. A priori we decided that included studies had to report a comparison between two or more chest compression rates and/or chest compression depths and/or measures of chest wall recoil and/or measures of chest wall leaning.
During the course of our searches, we identified a number of studies that presented means of a chest compression component for different outcome groups (e.g. mean chest compression rate in survivors to 30 days vs non-survivors). This did not fit precisely into the original PICO question but, being a scoping review, we ultimately made a pragmatic decision to include this data.
The chest compression components considered were:
- Chest compression depth: measured in millimetres, centimetres or inches
- Chest compression rate: measured in compressions per minute
- Chest wall recoil/leaning. Recoil is the sternum returning to its original position during the decompression phase of chest compressions. Leaning occurs when the rescuer fails to completely release pressure on the chest between chest compressions, which prevents full chest wall recoil
We included studies that reported any clinical outcome. We included studies reporting on adults or on infants and children, and we included studies reporting on out-of-hospital cardiac arrest (OHCA) or in-hospital cardiac arrest (IHCA), or both.
We excluded studies that provided continuous data linking a chest compression component to an outcome, unless two or more specific and comparable epochs were presented.
We excluded manikin studies and animal studies. We excluded studies that reported on pre- and post-shock pause in chest compressions and chest compression fraction.
We also did not include studies reporting on chest compression release velocity (CCRV). Although related to the concept of chest wall recoil / leaning, the TF ultimately felt that CCRV was a complex measurement that would be extremely difficult to modify in training or practice of Basic Life Support, particularly in the lay population.
Data Tables: BLS 2501 Defining chest compression components Data Tables SAC approved
These are presented in attached documents.
Table 1 shows studies that have reported a comparison between two or more chest compression components and the effect of this on a clinical or physiological outcome.
Table 2 shows studies that have reported two different measures of an outcome (e.g. ROSC vs no ROSC) and the mean values of a chest compression component in these groups.
Task Force Insights
1. WHY THIS TOPIC WAS REVIEWED
The three main components of chest compression – rate, depth and recoil – were reviewed as separate systematic reviews in the 2015 ILCOR CoSTR 4 5. The BLS Task Force subsequently decided to revisit this topic in 2019/2020 as a scoping review. The prior systematic search strategies were broadened to identify an evidence map evaluating the impact of these chest compression components i.e. rate, depth and recoil on outcomes individually and in interaction with each other 1.
However, the task force had not reviewed the topic since then. Three separate search strategies from the 2019/2020 Scoping Review (for each of depth, rate and recoil) have been updated / harmonized into one single search strategy. This corrects some minor discrepancies between the previous searches and has helped us to better identify studies which report on the interaction between two or more chest compression components.
2. Narrative summary of evidence identified
We included 39 studies in this review: 29 in adults (> 18 years) 3, 6-33 and 10 in infants and children 34-43. Twenty of those studies were in the 2019 scoping review – 17 in adults 6, 8, 9, 13-17, 19-21, 25, 27, 28, 30-32 and 3 in infants and children 38-40. We excluded two studies included in the 2019 scoping review, as they considered specifically chest compression release velocity 44, 45.
Chest compression rate
Adults
For the outcome of survival with favorable neurological outcome we identified one RCT 15 and three observational studies 7, 20, 32. The RCT reported no difference in survival with Cerebral Performance Category (CPC) 1-2 at rates of 100 vs 120/min (5.9% (8/136) vs 2.6% (4/156) p=0.154) (n=292 patients, all OHCA) 15. One OHCA observational study reported a significant increase in survival with a modified Rankin Score (mRS) <3 at rates 100-120 compared with 50-99/min (adjusted odds ratio, AOR: 100-120/min: 1.59 (95% CI 1.31-1.95), p<0.001) (n=22416) 7. A second OHCA study reported no difference in chest compression rate in survivors to hospital discharge with CPC 1-2 vs CPC 3-5 (113.3/min (95% CI 107.6-119.0) vs 112.8/min (95% CI 111.1-114.5) (n=418) 32. For IHCA, a single study reported no significant differences in survival with CPC < 3 for rates of 100-120/min, 121-140/min and >140/min (n=222) 20.
For the outcome of survival to hospital discharge / 30 days / one month we identified one RCT 15 and nine observational studies 16-18, 24, 29-33. One study reported survival to 30 days 18, one reported on both survival to 30 days and survival to hospital discharge 15 and all the others reported survival to hospital discharge only. The RCT reported no difference in either survival to hospital discharge or 30 days at a rate of 100/min vs 120/min (using a metronome prompt) (n=292, OHCA) 15. For OHCA, two observational studies reported no difference in survival to hospital discharge for: <80/min vs 80-140/min vs >140/min (n=3098) 16; ‘<80 or >120/min vs 80-120/min (n=12928) 33. One study reported an increase in survival to 30 days for chest compressions performed at 100-110/min vs <100/min (AOR 7.92 (95% CI 2.11-29.82), p=0.002) (n=181) 18. One OHCA study reported no differences in survival at rates <80 vs 80-99 vs 100-119 vs 120-139 vs >140/min in a model not adjusted for chest compression depth and fraction, but significantly worse outcome compared to the 100-119/min group in the 80-99/min group (AOR 0.73 (95% CI 0.57-0.93), p=0.011) and 120-139/min (AOR 0.63 (95% CI 0.45- 0.88), p=0.007) group in a model that did adjust for chest compression depth and fraction (n=10,371) 17. Four OHCA observational studies reported on the difference in chest compression rate in survivors vs non-survivors: two (n=9316 31 and n=1029 30, with possible overlap in populations) showing a statistically significant difference, albeit with rates differing by no more than 1/min between groups; two (n=181 18, and n=418 32) showed no statistically significant difference. One study reported no association between 10/min increases in chest compression rate and survival to hospital discharge(n=5547) 24. One study of both IHCA and OHCA, but not separating them out in the results, reported no difference in mean chest compression rate in those surviving to hospital discharge vs non-survivors (n=583: 227 IHCA and 356 OHCA) 29.
For the outcome of survival to Emergency Department (ED) admission (n=300) 9 and survival to hospital admission (n=284) 21 two observational studies in OHCA both reported no differences in chest compression rates in survivors vs non-survivors.
For the outcome of return of spontaneous return of circulation (ROSC) we identified one RCT 15 and nine observational studies 6 11 3 16 17 20 24 29 33. The RCT reported no difference in ROSC at a rate of 100/min vs 120/min (using a metronome prompt) (n=292, OHCA) 15. Five OHCA observational studies reported no association between chest compression rate and ROSC: ‘<80 or >120/min’ vs 80-120/min (n=2011 11 and n=12928 33), <80/min vs 80-140/min vs >140/min (n=3098) 16, <80/min vs 80-99/min vs 100-119/min vs 120-139/min vs >140/min (n=6399) 17; 10/min increases (n=5547) 24. One IHCA study reported significantly higher mean (standard deviation, SD) chest compression rates in those achieving ROSC vs not achieving (90/min (17) vs 79/min (18) (p=0.003) (n=97) 6. A second IHCA study reported better ROSC sustained for 20 mins for rates 121-140/min vs 100-120/min (AOR 4.48 (95% CI 1.42-14.14), p=0.010) (n=222) 20. An OHCA study reported no difference in mean (SD) chest compression rates in those achieving ROSC vs not achieving (117.7/min (9.2) vs 113.8/min (8.3), p=0.118) (n=47, mean age 64) 3. One study of both IHCA and OHCA, but not separating them out in the results, reported no difference in mean chest compression rate in those achieving ROSC vs those not (n=227 IHCA, n=356 IHCA) 29.
For physiological outcomes we identified five studies reporting on end-tidal carbon dioxide (EtCO2) measurements; one of these studies also reported blood pressure measurements. An IHCA cross-over trial reported significantly higher mean (standard error, SE) EtCO2 at 120/min vs 80/min (15.0mmHg (1.8) vs 13.0mmHg (1.8), p<0.001) (n=23) 19. An OHCA cross-over trial reported no differences in EtCO2 following mechanical CPR performed at rates of 60/min vs 80/min vs 100/min vs 120/min vs 140/min. Systolic blood pressure during CPR was significantly higher at a rate of 60/min compared to all other rates, but there was no difference in diastolic blood pressure during CPR at any rate (n=18) 25. One OHCA observational study reported a significant increase in EtCO2 (1.7% (95% CI 0.2-3.1%), p=0.02) for every 10/min increase in chest compression rate starting from a baseline of 75.9/min (n=230) 23. Another OHCA study reported no overall association between CC rate increases of 10/min and EtCO2 (n=47, mean age 64) 3. One study of both IHCA and OHCA, but not separating them out in the results, reported no difference in EtCO2 for every 10/min increase in compression rate between 90/min and 130/min (n=227 IHCA, n=356 IHCA) 29.
One other study reported no association between mean chest compression rate and first shock success in ventricular fibrillation (VF) (n=60: n=27 IHCA, n=33 OHCA) 13.
Infants and Children
For the outcome of survival with favorable neurological outcome we identified one IHCA observational study that reported no difference in favorable neurological survival at hospital discharge (Pediatric Cerebral Performance Category (PCPC) 1-3 or no worsening from baseline) at chest compression rates 100-120/min versus ‘non-compliant’ (i.e. not 100-120/min). Sub-group analysis reported higher favorable neurological survival at chest compression rates of 80-99/min versus 100-120/min (aRR 2.12, 95% CI 1.09-4.13, p=0.027) but no difference for 120-140/min vs 100-120/min or >140/min vs 100-120/min (n=164, infants and children <19 years old) 38.
For the outcome of survival to hospital discharge, we identified one OHCA observational study 39 and two IHCA observational studies 38 34. The OHCA study reported no difference between ‘<100/min or >120/min’ vs 100-120/min groups (n=383, age 1-18 years) 39. The first IHCA study reported increased survival in the 80-99/min vs 100-120/min groups (aRR 1.92, 95% CI 1.13-3.29, p=0.017) and no differences between 121-140/min, 140+/min and overall ‘non-compliant’ chest compression rates vs 100-120/min (n=164, infants and children <19 years-old) 38. In the second IHCA study on a PICU, there was no difference in median CC rate in survivors to hospital discharge vs non-survivors: 121/min (IQR 112–130) vs 121/min (IQR 112–128), p=0.429 (n=413, 37 weeks to 18 years) 34.
For the outcome of survival at 24 hours, we identified one OHCA observational study that reported no difference between ‘<100/min or >120/min’ vs 100-120/min groups (n=383, age 1-18 years) 39.
For the outcome of ROSC, we identified one OHCA observational study 39 and one IHCA observational study 38. In the OHCA study there was no difference in adjusted analyses between ‘<100/min or >120/min’ and 100-120/min groups (n=390, age 1-18 years) 39. The IHCA study reported no differences between 80-99/min, 100-120/min, 121-140/min and 140+/min groups (n=164, infants and children <19 years-old) 38.
For physiological outcomes we identified five IHCA observational studies 38 41 42 37, 43. The first reported no differences in diastolic blood pressure during CPR between 80-100/min, 100-120/min, 120-140/min and >140/min groups. Rates >120-140/min, compared to rates of 100-120/min, were associated with a significant decrease in systolic blood pressure during CPR (point estimate −4.07, 95% CI −7.17 to −0.97, p=0.010) (n=164, infants and children <19 years-old) 38.
The second reported chest compression rates ≥100/min vs <100/min were significantly associated with systolic blood pressure during CPR ≥80mmHg (OR 1.32, 95% CI 1.04 to 1.66, p=0.02) and diastolic blood pressure during CPR ≥30mmHg (OR 2.15, 95% CI 1.65 to 2.80, p<0.001) (n=9, age 1 to <18 years old) 41. The third reported chest compression rate during epochs with EtCO2 > 15 mm Hg vs < 15mmHg was 108/min (IQR 93–120/min) vs 132/min (IQR 114–144/min) (p < 0.001) and EtCO2 was less than 15 mm Hg in 92% of epochs where CC rate was greater than 120 compressions per minute (n=17, age 1 to 17 years) 42. The fourth reported no significant differences in EtCO2 after one minute at rates of 140/min vs 100/min (p = ‘not significant’) (n=6, age 2-26 months) 43. The fifth study reported no difference in median chest compression rate in patients who achieved an average ETCO2 >20mmHg during the first 10 minutes of CPR vs those who achieved ETCO2 <20mmHg (117.7/min (IQR 108.8-125.5) vs 117.9/min (IQR 109.5-125.1), p=0.899) (n=181, age 37 weeks to 18 years) 37.
Chest compression depth
Adults
For the outcome survival with favorable neurological outcome we identified one OHCA observational study. There were no differences in survival at hospital discharge with CPC 1-2 for chest compression depths <38mm vs 38-50.9mm, nor any difference in mean chest compression depth between survivors with CPC 1-2 and survivors with CPC 3-5 (n=418) 32.
For the outcome survival to hospital discharge / 30 days / one month we identified five observational studies 18 24 30-32. One study reported survival to 30 days 18; all the others reported survival to hospital discharge. All concerned OHCA patients. Four studies compared chest compression depths of <38mm, 38-51mm and >51mm. One of these reported significantly worse outcomes with chest compression depths <38mm vs >51mm (AOR 0.69, 95% CI 0.53-0.90, n=9316) 31; the other three (n=5547 24, n=1029 30 and n=418 32) reported no differences. One of these studies also reported no differences between chest compression depths <50mm vs 50-60mm vs >60mm 24. Another study reported no difference in 30-day survival with depths <5cm vs > 5 cm (n=181) 18. Two studies reported increased chest compression depth in survivors compared to non survivors (mean (SD) 43.5mm (10.7) vs 41.8mm (11.8), p<0.001 31 and mean 53.6mm (95% CI 50.5-56.7) vs 48.8mm (95% CI 47.6-50.0) 32); two others reported no association 18 30. Two studies reported improved survival for every 5mm increase in chest compression depth – (AOR 1.04, 95% CI 1.00-1.08, p=0.045) 31 and AOR 1.29 (95% CI 1.00-1.65) 32. One other reported no association 30.
For the outcome survival to ED or hospital admission we identified one RCT 9 and three observational studies 21 30, 31, all concerning OHCA patients. Two studies (n=9136 31 and n=1029 30, likely overlapping cohorts) reported survival to the day after the OHCA for depths of <38mm vs 38-51mm vs >51mm. The latter reported reduced survival in the <38mm group vs >51mm group (AOR 0.71 (95% CI: 0.61-0.83)) 31; the earlier reported increased survival in the 38-51mm group vs the <38mm group (AOR 1.52 (95% CI: 1.06-2.18)) 30. These studies also reported on survival for every 5mm increase in depth (AOR 1.05 (95% CI 1.03-1.08), p<0.001 in the latter study 31 and AOR 1.08 (95% CI 0.99-1.18) 30 in the earlier study). Another study reported an increased survival to hospital admission for every 1mm increase in CC depth (AOR 1.05 (95% CI 1.01-1.09)) (n=284 21). One study reported no difference in chest compression depth in survivors to ED admission vs non-survivors (n=300) 9.
For the outcome ROSC we identified five observational studies, all concerning OHCA patients 8 24 31 30 3. Two studies (n=9136 31 and n=1029 30, likely overlapping cohorts) reported pre-hospital ROSC for depths of <38mm vs 38-51mm vs >51mm. The latter reported reduced ROSC in the <38mm and 38-51mm group vs >51mm group (<38mm AOR 0.70 (95% CI: 0.60-0.80); 38-51mm AOR 0.86 (95% CI: 0.75-0.97), p<0.01 for overall association)31; the earlier reported no difference in ROSC between groups 30. These studies also reported on pre-hospital ROSC rates for every 5mm increase in depth (AOR 1.06 (95% CI 1.04-1.08), p<0.001 in the latter study 31 and AOR 1.05 (95% CI 0.98-1.14) in the earlier study 30). One study reported increased ROSC at ED arrival for depth >51mm vs <38mm (AOR 1.21 (95% CI 1.01-1.47)) (n=5547) 24. One study reported no difference in transient ROSC (at least 30s of organised rhythm) in patients receiving at least one shock (n=202) for depths <4.78 and >4.78cm (7.9% (8/101) vs 16.8% (17/101), p=0.124), but a significant difference in patients whose resuscitation effort lasted at least 5 mins (n=126) for depths <5cm vs >5cm (8% (5/63) vs 24% (15/63), p=0.008) 8. One study reported no difference in mean (SD) chest compression depth in those achieving ROSC vs not achieving (57.5mm (11.7) vs 57.5mm (9.2), p=0.997) (n=47) 3.
For physiological outcomes we identified three observational studies reporting on EtCO2 measurements 3 23 29, all showing significant increases in EtCO2 for every 10mm increase in depth. One study reported an overall increase in EtCO2 per 10mm depth increase of 4.0% (95% CI 2.3-5.8%), p<0.0001 (n=230) – this was 6.5% (95% CI 3.1-10.0%), p=0.0002 for shockable rhythms (n=60) and 3.2% (95% CI 1.1-5.2%), p=0.0021 for non-shockable rhythms (n=170) 23. The second study reported an increase in EtCO2 per 10mm depth increase of 1.4mmHg, p<0.001 for all cases (n=583) – this was 1.3mmHg, p<0.001 for IHCA (n=227) and 1.7mmHg, p<0.001 for OHCA (n=336) 29. The third study reported an increase in EtCO2 per 10mm depth increase of 1.5mmHg, p<0.001 for all cases (n=47) – this was 2.2mmHg, p<0.001 for shockable rhythms (n=11) and 1.5mmHg, p=0.056 for non-shockable rhythms (n=36) 3.
For other outcomes one observational study reported an increased mean (SD) chest compression depth in successful vs unsuccessful first shock (39mm (11) vs 29mm (10), p=0.004) and an increase in first shock success for every 5mm increase in chest compression depth (AOR 1.99 (95% CI 1.08-3.66), p=0.028) (n=27 IHCA, n=33 OHCA) 13. An IHCA observational study reported greater mean chest compression depth (56mm vs 52mm, p=0.04) and peak chest compression depth (77mm vs 70mm, p=0.003) in a group receiving CPR-related injury vs no injury. The proportion of those injured at mean depths of <50mm vs 50-60mm vs >60mm was 28% vs 27% vs 49%, p=0.06) (n=170) 14
Infants and Children
For the outcome of survival with favorable neurological outcome at hospital discharge we identified two IHCA studies 35, 40. One study was a secondary analysis of a parallel, stepped wedge, hybrid cluster randomized interventional trial. The study reported no differences between ≥40 mm vs <40mm (for age <1 year) and ≥50 mm vs <50 mm (for age ≥1 year) in those discharged with paediatric CPC of 1-3 or no worse than baseline, paediatric CPC of 1-3 or no worse than baseline or survival to hospital discharge with no new co-morbidities (n=114, infants and children <19 years) 35. An observational study reported no difference in survival to hospital discharge with paediatric CPC 1-2 in patients where >60% of 30-second chest compression epochs were ≥51mm (vs <51mm as reference) (n=78, age 1-18 years) 40.
For the outcome of survival to hospital discharge, we identified two IHCA 35, 40 and one OHCA 39 study. One IHCA study was a secondary analysis of a parallel, stepped wedge, hybrid cluster randomized interventional trial. The study reported no differences between ≥40 mm vs <40mm (for age <1 year) and ≥50 mm vs <50 mm (for age ≥1 year) (n=114, infants and children < 19 years) 35. An IHCA observational study reported no difference in survival to hospital discharge in groups where >60% of 30-second chest compression epochs were ≥51mm (vs <51mm as reference) (n=78, age 1-18 years) 40. An OHCA observational study reported no difference in survival to hospital discharge in unadjusted analyses when mean chest compression depth was ≥38mm vs <38mm (n=153, 1-18 years) 39.
For the outcome of survival at 24 hours we identified one observational IHCA study 40 and one observational OHCA study 39. The IHCA study reported significant increased survival at 24 hours in patients where >60% of 30-second chest compression epochs were ≥51mm (vs <51mm as reference) (AOR 10.3, 95% CI 2.75-38.8, p<0.001) (n=78, age 1-18 years) 40. The OHCA study reported no difference in survival to 24hrs in unadjusted analyses when mean chest compression depth was ≥38mm vs <38mm (n=153, 1-18 years) 39.
For the outcome of ROSC we identified two IHCA studies 35, 40 and one observational OHCA 39 study. One IHCA study was a secondary analysis of a parallel, stepped wedge, hybrid cluster randomised interventional trial. The study reported no significant differences between ≥40 mm vs <40mm (for age < 1 year) and ≥50 mm vs <50 mm (for age ≥ 1 year) in ROSC for >20 minutes (n=114, infants and children <19 years) 35. An observational IHCA study reported significant increased ROSC in patients where >60% of 30-second chest compression epochs were ≥51mm (vs <51mm as reference) (AOR 4.21, 95% CI 1.34-13.2, p=0.014) (n=78, age 1-18 years) 40. The OHCA study reported no difference in ROSC in adjusted analyses when mean chest compression depth was ≥38mm vs <38mm (n=153, 1-18 years) 39.
For physiological outcomes we identified three observational IHCA studies 36, 37, 41. One study reported that chest compressions approximating 1/2 anterior-posterior chest depth vs 1/3 anterior-posterior chest depth had higher (mean) systolic blood pressure during CPR (83.4mmHg versus. 51.6mmHg, p<0.001), mean arterial pressure (48.0mmHg vs 37.5mmHg, p<0.001) and pulse pressure (52.9mmHg vs 21.0mmHg, p < 0.00), with no differences in mean diastolic blood pressure during CPR (n=6, age 2 weeks to 7.3 months, IHCA post-cardiac surgery) 36. The second study reported that in patients with average chest compression depth ≥38mm (vs <38mm) there was no difference in the number of patients with systolic blood pressure during CPR >80 mmHg or diastolic blood pressure during CPR >30 mmHg (n=9, age 1.75-17 years on PICU) 41. The third study reported no difference in median chest compression depth in patients who achieved an average ETCO2 >20mmHg during the first 10 minutes of CPR vs those who achieved ETCO2 <20mmHg: 34.26mm (95% CI 24.75-45.21) vs 32.10mm (95% CI 21.82-53.70), p=0.960 (n=181, age 37 weeks to 18 years) 37.
Recoil/leaning
We did not identify any studies in adults or in infants and children that reported on the association between recoil/leaning and outcome.
Interactions
Adults
For the outcome survival with favorable neurological outcome we identified four observational studies 10 12 26, 27, all concerning OHCA patients. One observational study compared American Heart Association (AHA) compliant chest compressions (defined as: mean values for at least 70% of the first 10 minutes of CPR were: rate 100-120, depth 50-60mm, chest compression fraction >80%, pre-shock pause <10s). In a model including chest compression rate, depth and fraction AOR for survival with MRS < 3 (compliant vs non-compliant chest compressions) was non-significant overall: 1.42 (95% CI 0.73-2.74). However, there was a significant improvement in survival with MRS < 3 in the subset (n=3597) who achieved ROSC only after >10 minutes of CPR (3.03 (95% CI 1.12-8.20) (n=18,359) 10. A second study reported improved survival with MRS < 3 in those receiving chest compressions within 20% of ‘optimum’ values (rate 107/min and depth 3.8-5.6cm) vs those receiving non-optimum compressions (OR 1.44 (95%CI 1.07-1.94), p=0.02) (n=3643) 12. The third, which compared ‘high-quality’ bystander CPR (CC rate ≥100/min and CC depth ≥50 mm with appropriate hand position) (n=149) vs ‘low quality’ bystander CPR (not meeting the ‘high-quality CPR’ definition) (n=2342), reported significant improvements in survival with CPC 1-2 in the ‘high-quality’ group (25.5% (38/149) vs 5.7% (134/2342), p<0.001) 26 The fourth (a before-and-after study) reported no difference in survival to 30 days with CPC 1-2 following the introduction of real-time audiovisual feedback, despite significant differences in rate and depth (mean (SD) values before: rate 139.9/min (8.9) and 38.8mm (11.5) vs after: rate 117.2 (7.4) and depth 48.0mm (9.2) (n=32) 27.
For the outcome survival to hospital discharge / 30 days / one month we identified four observational studies 10, 24, 26, 27, all concerning OHCA patients. One reported survival to 30 days 27, the others survival to hospital discharge. One observational study compared American Heart Association (AHA) compliant chest compressions (as above). There was no significant improvement vs non-compliant compressions in either a model including chest compression rate, depth and fraction (n=18,359) or in a model including chest compression rate, depth, and fraction and pre-shock pause (n=3520). However, there was a significant improvement in survival to hospital discharge in the subset (n=4158) who achieved ROSC only after >10 minutes of CPR (model including chest compression rate, depth and fraction: AOR 2.17 (95% CI 1.11-4.27) 10. A second paper compared multiple combinations of chest compression rate (<100/min, 101-120/min, 121-140/min, >140/min) and depth (<38mm, 38-51mm, >51mm). None of the combinations were associated with differences in survival to hospital discharge compared to the reference of chest compression rate < 100 and depth <38mm (n=5547) 24. The third, which compared ‘high-quality’ bystander CPR (n=149) vs ‘low quality’ bystander CPR) (n=2342) (as above), reported significant improvements in survival to hospital discharge in the ‘high-quality’ group (30.2% (45/149) vs 10.1% (236/2342), p<0.001) 26. The fourth (a before-and-after study) reported no difference in survival to 30 days following the introduction of real-time audiovisual feedback, despite significant differences in rate and depth (as above) 27.
For the outcome survival to 24 hours we identified one observational study in OHCA patients 27. This (before-and-after) study reported no difference ROSC following the introduction of real-time audiovisual feedback, despite significant differences in rate and depth (as above) 27.
For the outcome ROSC, we identified three observational studies 22 26 27. Two reported on OHCA patients 26 27 and one reported on cardiac arrest in ED patients 22. The ED paper reported that there was no difference in the proportion of patients who received ‘compliant’ chest compressions (defined as a rate 100-120/min and depth 5-6cm) in the group who achieved ROSC (n=17) and the group that did not (n=33) 22.
The first OHCA study, which compared ‘high-quality’ bystander CPR (n=149) vs ‘low quality’ bystander CPR) (n=2342) (as above), reported significant improvements in the ‘high-quality’ group for both pre-hospital ROSC (41.6% (62/149) vs 22.5% (528/2342), p<0.001) and ROSC at any time (47.7% (71/149) vs 29.0% (680/2342), p<0.001) 26. The second (before-and-after) OHCA study reported no difference in survival to 30 days following the introduction of real-time audiovisual feedback, despite significant differences in rate and depth (as above) 27.
For other outcomes we identified one paper reporting BP measurements 28 and one reporting EtCO2 29. Both papers reported on both IHCA and OHCA patients. One study compared multiple combinations of chest compression rate (<100/min, 100-120/min and >120/min) and depth (<50mm and > 50mm). Compared to the reference (<100/min and <50mm) almost all combinations resulted in significant higher odds of achieving both femoral (n=24, 20 IHCA, 4 OHCA) and radial (n=15, all IHCA) arterial systolic blood pressure during CPR of >85mmHg and radial arterial diastolic blood pressure during CPR of > 30mmHg during CPR. The odds of achieving femoral arterial diastolic blood pressure during CPR of >30mmHg were increased for the combination of <100/min and >50mm and significantly decreased for all other combinations 28. The second study reported that, at five pre-specified chest compression rates, a 10mm increase in chest compression depth was associated with increases in EtCO2. At five pre-specified chest compression depths, a 10/min increase in rate was not associated with increases in EtCO2 (n=583: 227 IHCA, 356 OHCA) 29.
Infants and Children
There were no studies in infants and children that reported on the effect of interactions between depth, rate, and recoil on clinical outcomes.
For physiological outcomes we identified one observational IHCA study. Patients receiving chest compressions >100/minute and > 38mm depth (vs <100/min and <38mm depth were more likely to achieve a systolic blood pressure during CPR of >80mmHg (OR 2.02, 95% CI 1.45-2.82, p<0.001) and a diastolic blood pressure during CPR of >30mmHg (OR 1.48, 95% CI 1.01-2.15, p=0.042) (n=9, 1.75-17 years, in PICU) 41.
3. Narrative Reporting of the task force discussions
This scoping review demonstrated that most studies focused on a single chest compression component, and several studies suggest the presence of confounding interactions that should prompt caution when evaluating any chest compression component in isolation.
Most studies are observational – where we identified randomized trials, the chest compression components were not the variables primarily being investigated. Most adult studies identified in this review were focused on out-of-hospital cardiac arrest. Studies in infants and children, however, were predominantly from in-hospital studies. Studies are heterogeneous and making direct comparisons between studies is difficult. There is a lack of consistency in results between studies.
Early pediatric clinical studies that shaped existing chest compression guidance relied on single-sensor CPR quality monitors, which may have overestimated compression depth because measurements could be influenced by non-rigid surfaces and patient movement during compressions 39, 40. In contrast, more recent observational studies using advanced dual-sensor (anterior and posterior) feedback devices have found that recommended pediatric compression depth targets are seldom achieved in clinical settings, especially for infants 34, 46, 47. These dual-sensor systems measure the displacement between two sensors rather than overall movement of the device and patient, reducing artifact from surface compliance and motion.
This expanded scoping review identified sufficient new evidence to prioritize updating the 2015 systematic reviews and the Consensus on Science and Treatment Recommendations; however, to ensure continuity and usability of international guidance on the core components of CPR, the existing treatment recommendations remain in place while SR updates are undertaken.
Prior treatment recommendations in adults (2015):
- We recommend a manual chest compression rate of 100 to 120/min (strong recommendation, very-low certainty evidence).
- We recommend a chest compression depth of approximately 5 cm (2 in) (strong recommendation, low certainty evidence) while avoiding excessive chest compression depths (greater than 6 cm [greater than 2.4 in an average adult) during manual CPR (weak recommendation, low-certainty evidence).
- We suggest that rescuers performing manual CPR avoid leaning on the chest between compressions to allow full chest wall recoil (weak recommendation, very low-certainty evidence).
Prior treatment recommendations in children (2015):
- We suggest that rescuers compress the chests of infants by at least one third the anterior-posterior dimension, or approximately 1½ inches (4 cm). We suggest that rescuers compress the child’s chest by at least one third of the anterior-posterior dimension, or approximately 2 inches (5 cm) (weak recommendation, very-low-quality evidence).
Based on the results of this scoping review and the apriori decision of the Paediatric Life Support Taskforce to use adult data as indirect evidence for compression rate the PLS TF have prepared a Good Practice Statement in the interim until the systematic review and CoSTR can be updated.
The target for manual chest compression rate may be 100 to 120/min for infants and children in cardiac arrest (Good Practice Statement).
EtD: BLS 2501 Defining chest compression components rate depth recoil Sc R Et D SAC approved
Knowledge Gaps
There is a paucity of studies and trials for infants and children in cardiac arrest comparing clinical outcomes for compression rate and depth and recoil or leaning and on the effect of interactions between rate, depth and recoil.
There is insufficient evidence from studies in infants and children to determine the appropriate chest compression depth based on patient weight or size.
There is no evidence on clinical outcomes evaluating measured depth compression using a feedback device compared with estimated depth based on changes in the anterior-posterior chest diameter.
Further clinical studies employing dual-sensor technology that correlate compression metrics with P-COSCA 2 outcomes are needed to better define optimal targets for compression depth, rate, and recoil in infants and children.
There is a lack of evidence about the effect of leaning and recoil on clinical outcomes.
There is a lack of randomized trials or high-quality evidence related to chest compression components on critical and important clinical outcomes, particularly considering the interaction between these components.
In this review we excluded papers reporting continuous data about chest compression rate and depth, and the association with clinical and physiological outcomes. We can therefore make no comment about the best combination of chest compression rate and depth during CPR.
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