More than 20,000 pediatric cardiac arrests occur in the United States each year. Overall, outcomes for pediatric out-of-hospital cardiac arrest (POHCA) remain dismal and have had no substantial improvements for decades. Until recently the best rate observed in data for survival to hospital discharge following POHCA has been 11.4% (only 4.9% for infants). A recent report from high-functioning systems found rates between 6.7%–10.1%. More concerning, unfavorable neurologic outcomes are reported in the majority of pediatric arrest survivors. Most functional survivors are found among in-hospital pediatric patients.1
Why haven’t infants and children who experience cardiac arrest outside the hospital benefited from the rigorous contributions made by so many resuscitation scientists over so many years? This same question was asked in 2011, six years after the release of the 2005 PALS guidelines, when investigators found cardiac arrest survival had not improved in the Resuscitation Outcomes Consortium (ROC). Translation of science to the field was often delayed—taking 17 months on average, in one analysis, to achieve a compliance of 80%.2
In one more attempt to move the needle on outcomes, the 2020 PALS guidelines follow a 2019 update, released in a follow-through on the PALS committee’s goals of shortening the release cycle, expanding their algorithmic reach, and increasing the frequency of educational encounters.
Simply stated, we have not made much headway in decades with respect to improving neurologically intact outcomes for kids, particularly with out of-hospital cardiac arrests. Survival from pediatric in-hospital cardiac arrest (PIHCA) has improved, yet the same cannot be said about POHCA. While the etiologies, technologies, and interventional factors available in-hospital may be advantageous, the results for POHCA remain disappointing, as noted in the October 2020 guidelines publication in Circulation.
“Survival rates from OHCA remain less encouraging. In a recent analysis of the Resuscitation Outcomes Consortium Epidemiological Registry, a multicenter OHCA registry, annual survival to hospital discharge of pediatric OHCA between 2007 and 2012 ranged from 6.7% to 10.2% depending on region and patient age. There was no significant change in these rates over time, consistent with other national registries.”1
Still, credit goes to the writing committee for expanding the educational offerings to different aspects of basic and advanced life support and recognizing that biennial training is not the ideal strategy.
In this editorial I will focus on POHCA and review the two key changes to the 2020 guidelines that raised questions for me from the perspective of an EMS medical director and pediatric emergency medicine physician.
Key Change #1
A respiratory rate of 20 to 30 breaths per minute is new for infants and children who are (a) receiving CPR with an advanced airway in place or (b) receiving rescue breathing and have a pulse.1
This recommendation is a significant departure from prior guidelines, where the ventilation rate for all children (and adults) in cardiac arrest was 10 positive-pressure breaths per minute, or one breath every six seconds. The new recommendation of 20–30 is 2–3 times higher than prior recommendations and pushes back against decades-old scientific and physiologic studies concerning intrathoracic pressure regulation.
In 2004 a landmark paper reported the effect of varying positive-pressure ventilation rates (12, 20, and 30 bpm) on groups of juvenile pigs in cardiac arrest.3 The authors found excessive ventilation rates significantly decreased coronary perfusion pressures, increased mean intratracheal pressures, and negatively impacted survival. Six of the seven pigs in the 12-bpm group survived, compared to only one in each of the other groups (p = 0.06).
Those findings in pigs, inspired by observing excessive ventilation rates in humans during CPR, identified the physiological mechanism underlying the harmful effects of ventilation rates of 20 or 30 during CPR. Specifically, with each positive-pressure breath, venous return was inhibited, and intracranial pressure was increased. With 10 breaths per minute, nearly all pigs survived, whereas with 30 breaths per minute, nearly all pigs died.
Further work in recent years demonstrated that excessive ventilation impedes cerebral perfusion, a more concerning sequela that may further explain the poor POHCA outcomes documented in national registries. Not only are children with POHCA (versus PIHCA) very often dehydrated, they may also have fever or sepsis that may further exacerbate preload reduction and worsen the impact of hemodynamic compromise.
Also, with the focus on children having respiratory etiologies for their arrest, practices have evolved to “breathe more” even when the condition has progressed to cardiac arrest, indicating a different physiological condition. This additional, poorly monitored habit is also augmented by anxious rescuers.
Between 2013 and 2016, the Collaborative Pediatric Critical Care Research Network sought to evaluate the effect of ventilation rates during CPR across several hospitals. The results of this PIHCA study informed the change to the 2020 guidelines. This single in-hospital study involved 47 pediatric ICU patients who all had advanced airways in place prior to their arrest, and 60% had congenital heart disease documented as a preexisting condition.4 Presumptively these children were being monitored, and their preload status was being managed. Notably, 74% had a first documented rhythm of bradycardia with poor perfusion, not the typical asystolic state with which the POHCA population presents, and a condition indicating a more profound cardiovascular collapse and even poorer survival chances. In this PICHA study, all eight patients presenting in asystole died.
In my opinion, this single study should not necessarily apply to the POHCA patient. The physiologic effects of the new recommendation will surely have detrimental consequences in the out-of-hospital setting, especially with what is already known about the cardiac arrest pressure and flow challenges that occur during CPR.
Cerebral oxygenation and perfusion matter most during cardiopulmonary resuscitation, forcing the strategies we employ to be hyperfocused on the flow of oxygenated blood into (and out of) the cerebral vessels. Elevated intrathoracic pressures from too much positive-pressure ventilation and chest compression can raise intracranial pressure and inhibit flow. Flow and in and out of the lungs’ blood vessels (through which the entire circulation passes) is equally important. Frequent positive-pressure ventilations may not only lead to vasoconstriction of cerebral vessels but can also reduce right ventricular filling by obstructing preload. An occasional large inflation or two is clearly in order to ensure adequate recruitment of dependent lungs during compressions and reduce pulmonary vascular resistance due to atelectatic regions that can close off blood flow. However, frequent breaths, and particularly low-volume breaths that do not ensure adequate lung inflation, can be doubly detrimental. Animal models demonstrated this physiology decades ago, and it is still supported by Dr. Johanna Moore’s groundbreaking data on heads-up positioning during cardiac arrest.5
Claiming there are no pediatric data to prove that 10 bpm (or fewer) is the correct ventilation rate simply doesn’t pass the physiologic sniff test. The earlier-mentioned piglet studies based on the physiology of intrathoracic pressure control resulted in the strong recommendation in the 2005 adult BLS AHA guidelines to limit positive-pressure ventilations to around 10 per minute at best.6 In my opinion no new data exist today to justify changing those important prior recommendations for POHCA. The new recommendations would only increase the likelihood of harm for POHCA patients.
Strengthening this case further is the recent study by Paul Banerjee, et al., published in 2019 and likely not taken into account in the new guidelines. In that quality improvement project, responders to POHCA provided rapid intraosseous access and adrenaline, an immediate advanced airway, and quality CPR (all on scene) and also controlled breathing to one large positive-pressure breath (enough to elevate the chest wall)—and then did not provide additional breaths for 10 seconds or so (6 bpm).7 The strategy was that the large tidal volume represented a more efficient breath for oxygenation, ventilation, and better blood flow through the lungs. Frequent rates were not needed, and frequent intrathoracic pressure swings were avoided. Neurologically intact survival was dramatically improved well beyond the statistics first quoted here. Although it was a part of bundled approach to care, investigators asserted that all the components, including the ventilatory strategy, were needed to get the compelling result.
It deserves mention that the 2020 International Liaison Committee on Resuscitation (ILCOR) Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care did not modify its recommendation to 20–30 bpm, choosing instead to wait for more data on the topic.8 I remain strongly in that camp.
Key (Non-)Change #2
If bradycardia persists after a correction of other factors (e.g., hypoxia) or responds only transiently, give epinephrine IV/IO.1
While this headline was surely buried for non-CPR junkies, this nonchange regarding the use of epinephrine in symptomatic bradycardia was disappointing. There is evidence that giving cardiac arrest-dose epinephrine to someone with a pulse can be detrimental to the “pump” itself. This illustrates the double-edged sword of epinephrine and partly suggests why it’s being peeled away from the shockable rhythm pathway.
Cardiac arrest-dose epinephrine is not recommended in ACLS, yet it has lingered in the pediatric guidelines for decades, much to my chagrin.9 So when Dr. Mathias Holmberg’s 2019 paper was published in Resuscitation, I was elated. It finally put the last nail in the coffin for this recommendation—or so I thought.
In the study a total of 3,528 patients with bradycardia with poor perfusion (a nonpulseless event) received epinephrine and were matched to 3,528 patients at risk of receiving epinephrine based on a propensity score. The authors found administration of epinephrine was associated with decreased survival to hospital discharge, ROSC, 24-hour survival, and favorable neurologic outcome.10 Epinephrine was also associated with an increased risk of progression to pulselessness. The 2020 PALS writing group acknowledged this paper, yet chose not to “go with the flow,” stating the study had limitations and further research was required.
Let’s be clear: I’m not against epinephrine; I’m simply against the dose and mechanism of administration (IVP). It’s important to understand that using the 100 mcg/mL concentration of epinephrine at 0.01 mg/kg (cardiac arrest dose) in a child, or 1 mg in a healthy adult, leads to increased oxygen demand, elevated systemic vascular resistance, and ultimately myocardial ischemia. Based on the physiology and convincing Holmberg data, my EMS protocols now use push pressor epinephrine (10 mcg/mL) for bradycardia with poor perfusion at a dose of 1 mL (10 mcg) every minute PRN, titrated to effect. It’s akin to drinking a margarita instead of a straight shot of tequila.
Where Do We Go From Here?
Over the last decade the EMS community has recognized that successful resuscitation relies heavily on three important factors: bystander CPR, telephone CPR (T-CPR), and on-scene high-performance (HP) CPR. Each of these critical steps is hyperlocal, meaning individual communities must put in the work to make them come to life. Dedicate someone on your team to work intimately with dispatch, another to go from station to station to train on HP-CPR, and then review the key metrics (compression and ventilation rates, pauses) after every call in a nonpunitive manner. This is the key to the concept of the “bundle,” something the Take Heart America group has proven and recently published.11
A review of cities with the best OHCA outcomes reveals each has dedicated a significant amount of time to each of the three pillars. And while bystander CPR and T-CPR are out of the scope of this editorial, make no mistake that their role is just as important as high-quality on-scene resuscitation. HP-CPR can best be described as the final mile of an Amazon delivery: It’s the final step in an already-complicated process, but often the most difficult. Getting that package to your door when the warehouse is only a mile away is quite complex.
This same argument can be made for a HP-CPR sequence: Merely telling a provider to push on the chest 110 times per minute and ventilate once every six seconds is like staring at a brown box on the shelf in an Amazon warehouse and telling it to find the correct doorstep. It doesn’t happen that easily—it takes work, but more importantly it takes people. It’s something only a small fraction of EMS systems have proven they can accurately accomplish. Why? Because the final mile of resuscitation requires persistence, departmentwide dedication, and continuous quality improvement until the results become apparent.
POHCA success, as with adult OHCA, cannot be approached in a silo. Making a single change to an arrest protocol will not impact outcomes—it’s all about the bundle. In the Amazon analogy, the package gets to your door the same day you ordered it not because of one small change, but because of the many logistical processes that work synchronously with, and rely intimately on, each other.
Let’s resist the search for the silver bullet that will magically improve POHCA outcomes and instead stay focused on maximizing the physiologic parameters of the two most important organs. While the heart is more resilient to anoxia, we can’t say the same for the brain. This forces us to stick to the foundational physiologic principles we know to be true.
It is our responsibility to continuously review the science as it is published, evaluate all published guidelines, then implement a system of high-performance care that shows a demonstrable impact in our communities. It is also our responsibility to speak up when there is a major change in the guidelines that flies in the face of well-accepted physiologic principles.
Every EMS medical director needs to be able to show their version of HP-CPR is working in their community and be committed to a rigorous and consistent CQI program that pays attention to every detail as if lives depend on it—because they do. We owe it to ourselves and to our community to get this right.
1. Topjian AA, Raymond TT, Atkins D, et al.; Pediatric Basic and Advanced Life Support Collaborators. Part 4: Pediatric Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 2020 Oct 20; 142(16_suppl_2): S469–S523.
2. Bigham BL, Koprowicz K, Rea T, et al. Cardiac arrest survival did not increase in the Resuscitation Outcomes Consortium after implementation of the 2005 AHA CPR and ECC guidelines. Resuscitation, 2011; 82(8): 979–83.
3. Aufderheide TP, Lurie KG. Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med, 2004 Sep; 32(9 Suppl): S345–S351.
4. Sutton RM, Reeder RW, Landis WP, et al.; Eunice Kennedy Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network (CPCCRN). Ventilation Rates and Pediatric In-Hospital Cardiac Arrest Survival Outcomes. Crit Care Med, 2019 Nov; 47(11): 1,627–36.
5. Moore JC, Holley J, Segal N, et al. Consistent head up cardiopulmonary resuscitation haemodynamics are observed across porcine and human cadaver translational models. Resuscitation, 2018 Nov; 132: 133–9.
6. American Heart Association. 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: pediatric basic life support. Pediatrics, 2006 May; 117(5): e989–e1,004.
7. Banerjee PR, Ganti L, Pepe PE, Singh A, Roka A, Vittone RA. Early On-Scene Management of Pediatric Out-of-Hospital Cardiac Arrest Can Result in Improved Likelihood for Neurologically-Intact Survival. Resuscitation, 2019 Feb; 135: 162–7.
8. Maconochie IK, Aickin R, Hazinski MF, et al.; Pediatric Life Support Collaborators. Pediatric Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation, 2020 Nov; 156: A120–A155.
9. Berg KM, Soar J, Andersen LW, 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 Oct 20; 142(16_suppl_1): S92–S139.
10. Holmberg MJ, Ross CE, Yankama T, Roberts JS, Andersen LW; American Heart Association’s Get With The Guidelines–Resuscitation Investigators. Epinephrine in children receiving cardiopulmonary resuscitation for bradycardia with poor perfusion. Resuscitation, 2020 Apr; 149: 180–90.
11. Pepe PE, Aufderheide TP, Lamhaut L, et al. Rationale and Strategies for Development of an Optimal Bundle of Management for Cardiac Arrest. Crit Care Explor, 2020 Oct 15; 2(10): e0214.
Peter Antevy, MD, is an EMS medical director for Coral Springs-Parkland Fire Department, Davie Fire Rescue, Southwest Ranches, and MCT Express in Florida, as well as medical director of pediatrics for Palm Beach County Fire Rescue. Antevy serves as medical director at the Coral Springs Institute of Public Safety and Broward College’s EMS program and is a pediatric emergency medicine physician at Joe DiMaggio Children’s Hospital. He is founder and chief medical officer of Handtevy–Pediatric Emergency Standards, Inc. Reach him at email@example.com.