Post ROSC care

Cite this article as:
Costas Kanaris. Post ROSC care, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.29109

Or some pointers on clinical management following the successful return of spontaneous circulation in children. 

It’s 5:40 am at Bubblesville ED. The red phone rings. The paramedic crew informs you that they are five minutes away with a 7 kg, 6-month-old, previously thriving, baby boy called Tarquin. He has had a witnessed out of hospital cardiac arrest at home and there was no prodromal illness according to the family. He choked during a breastfeed, turned blue, and stopped breathing. He had 5 minutes of CPR by the parents by the time the ambulance arrived and had ROSC by the paramedic team after a further 8 minutes. The rhythm strip was consistent with a PEA arrest. They are hand-ventilating him through an LMA.

This is his capillary gas on arrival in the ED
  1. What are your clinical priorities?
  2. What clinical problems do you anticipate in the immediate post-arrest phase?
  3. Who do you call for help?
  4. What do you do with the family whilst you’re managing the patient?
  5. What investigations do you need?

A systematic, collaborative, well-led approach to advanced paediatric life support can maximize the chances of the clinical team achieving a return of spontaneous circulation in a child that has arrested. We’ve seen the drill be before. We can go through our algorithms expertly and the 5-H’s and 5-T’s roll off the tongue, even under duress. The return of a pulse is heralded as the “hallelujah moment”, almost as if the patient is now healthy and safe and all we have to do is wait for the paediatric critical care retrieval team to arrive.

Whilst traditional APLS teachings are vital for the dissemination of knowledge and it’s application in everyday clinical life, their main focus is on the initial phase of achieving a pulse with very little attention placed on the all-important post-resuscitation phase.  This part of care is crucial, not only if we are to minimize secondary brain injury to the child but also to improve the chances of permanent returns of spontaneous circulation. Good short and long term outcomes rely heavily on how well we manage the post-resuscitation stage. 

There are four phases of cardiac arrest:-

Phase one: Prevention. This is the pre-arrest phase. Child safety and injury prevention strategies are in place to recognize deterioration. Adequate monitoring by using early warning systems and a pro-active approach to management is likely to contribute to avoiding an arrest.

Phase two: No flow arrest. This is a period of cardiac arrest prior to us commencing CPR. Our aim here is to minimize the time it takes to start life support. It is key that we involve the cardiac arrest team quickly, we start chest compressions early, and that we do not delay defibrillation if this is needed. 

Phase three: Low flow resuscitation. This phase describes when CPR is in progress. The aim is to achieve high-quality CPR in order to allow adequate coronary and cerebellar perfusion. Maintaining good ventilation and oxygenation whilst avoiding aggressive over-ventilation is paramount. It is during this phase that we systematically approach and threaten the reversible causes of cardiac arrest. 

Phase four: This is the post-resuscitation phase after ROSC has been achieved. Our aim here is to optimize coronary and cerebral perfusion. Neuroprotection and treatment of arrhythmias as well as treatment of post-cardiac arrest syndrome come under this phase. 

Adult v paediatric arrest: What’s the difference?

Out of hospital cardiac arrests in children >16 years of age are relatively rare – reported at 8-20/100000/ year. The incidence is only comparable to that of the adult population, estimated at 70/100000/year. The incidence of in-hospital paediatric arrests is much higher, with a nearly one-hundred-fold increase, compared to the out-of-hospital incidence for the <16’s. 

Survival, and especially a “good” survival from a neurological perspective still remain poor. Out of hospital survival rates are estimated to be 5 – 12%. Only 0.3 to 4% of those that survive have no long-term neurological insult.

Children have cardiac arrests due to severe respiratory insult or circulatory collapse, in the main. Either can lead to a respiratory arrest coupled with hypoxia, which then results in a cardiac arrest. The overwhelming majority of cardiac arrests present with a non-shockable rhythm.  It is also worth noting that almost half of the paediatric population that have a cardiac arrest have other chronic comorbidities such as respiratory conditions e.g. asthma, congenital cardiac disorders, or neurodisability. 

In the adult population, cardiac arrest is more likely due to long-term comorbidities such as ischaemic heart disease. This contributes to the development of an acute myocardial insult and (usually) a shockable rhythm. Understanding the difference in pathology leading to a cardiac arrest between adults and children is vital. Reversing the cause of the respiratory compromise can make the impalpable pulse palpable, allowing us to perfuse our patient once again. 

The recommended CPR ratio of 15:2 for children aims to provide adequate ventilation for oxygenation as well as satisfactory cardiac compressions to maintain sufficient perfusion of the coronary and cerebral circulation. Adult studies looking at compression-only CPR in patients with VF arrest have shown that success in achieving ROSC is due to pre-existing pre-arrest aortic blood oxygen and pulmonary oxygen stores.  As a mere 14% of cardiac arrests are due to a shockable rhythm, combining ventilation and compressions is vital. 

What is the Post Cardiac Arrest Syndrome (PCAS)? 

PCAS describes the period in which our patients are at the highest risk of developing ventricular arrhythmias and reperfusion injuries after ROSC. This is secondary to prolonged ischaemia then reperfusion of vital organs, primarily the myocardium and central nervous system. Its systemic effects are not dissimilar to those encountered in severe sepsis. There are four stages to PCAS:

  • Immediate post-arrest – First 20 minutes. 
  • Early post-arrest – 20 minutes to 6-12 hours. 
  • Intermediate phase – 6-12 hours up to 72 hours.
  • Recovery phase – From 72h onwards. 

Neuroprotection

Even high-quality closed-chest CPR can only achieve 50% of normal cerebral blood flow at best. It is not a secret that the brain does not tolerate hypoxia or ischaemia, the effects on both of these processes are exponential during a cardiac arrest, the longer the downtime, the worse the neurological hit

The pathophysiological cascade for neurodegeneration following cardiac arrest is complex and multi-factorial. Following a hypoxic or ischaemic period the brain develops cerebral oedema and cerebral hyperaemia. There is impaired cerebral vascular reactivity and like any other organ trying to reperfuse, the post-ischaemic biochemical cascade is activated. All these factors contribute to a secondary brain injury. Of course, the duration of hypoxia will in large part dictate how severe the primary brain injury is and whether the patient is likely to survive or not. Brain injury can manifest as myoclonus, stroke, seizures, coma, or brain death. 

We can minimize the extent of secondary brain injury with simple proactive, neuroprotective measures:

  • Strict normothermia
  • Aggressive seizure prophylaxis
  • Avoiding hypoxia and hyperoxia
  • Tight circulatory monitoring and support
  • Patient position
  • Eucapnia and normoventilation
  • Vigilant glucose monitoring
  • Frequent neurological assessment, especially before the administration of anaesthetic agents and paralysis

Strict normothermia

Therapeutic hypothermia following a cardiac arrest during the intermediate phase (after VF in adults), as well as newborns with birth asphyxia, has shown some correlation with better neurological outcomes and reduced neurodisability.  Similarly, there is strong evidence linking core temperature above 38° with worse neurological outcomes in patients following cardiac arrest. There is a wide variation in practice in relation to therapeutic hypothermia.  Mild hypothermia after paediatric cardiac arrest is in the policy of some PICU’s. Patients are cooled to 33-34°C for 1 – 2 days and are then gradually rewarmed. Paralysis can be used as an adjunct to stop shivering. Temperatures below 32°C should be avoided as they are associated with worse survival, immunosuppression, arrhythmias, coagulopathies, and infections.  The decision to “cool” must be made early and in conjunction with your critical care transport team. You have many tools at your disposal to achieve this such as cold IV fluids, cooling blankets, and catheters. 

What is, and should be, more aggressively targeted is strict normothermia (temperatures between 36-37°C), and depending on local practice hypothermia can be targeted to 33-36°C. Avoidance of pyrexia is crucial. Fever can result in an increased metabolic demand of the brain. This contributes to more ischemic injury and more infarcts as the threshold for ischemia in the injured brain is lower than that of the normal brain. The brain can no longer auto-regulate the mismatch between cerebral blood flow and metabolic demand.

Aggressive seizure prophylaxis

Seizures after paediatric cardiac arrest can occur in up to 47% of cases. 35% of these can lead to refractory status epilepticus.  Whilst CFAM/EEG monitoring is unlikely to be available in your local PED, it is important to have a low threshold to administer a long-acting anti-epileptic or a continuous infusion of a short-acting medicine to prevent/avoid this from happening. Ideally, a continuous infusion of midazolam +/- levetiracetam (less arrhythmogenic than phenytoin but both will work) and standard national guidelines should be followed. 

Clues as to whether a patient is still fitting include:

  • Unexpected changes in the pupillary size (beware of the child that had atropine on induction with the “fixed dilated pupils”).
  • Sudden changes in BP or heart rate.  

If you have given a paralytic for intubation, do not fall into the trap of thinking that the patient is not seizing, only an EEG or CFAM can tell you that. It is better to err on the side of caution.

Avoiding hypoxia and hyperoxia

Avoiding hypoxia and hyperoxia are also key components in minimizing secondary brain injury.  Whilst hypoxia will further exacerbate secondary brain injury, hyperoxia  (PaO2 > 40 kPa) is also be associated with worse survival due to oxygen free-radical formation that can inactivate intracellular enzymes, damage DNA, and destroy lipid membranes. It is reasonable to have high concentration oxygen therapy during the low-flow resuscitation and early post-resuscitation phases (as the commonest causes are respiratory). In the subsequent phases, we should target oxygen saturations between 94 and 96% and be proactive in how we reduce the FiO2 whilst avoiding hypoxia. There is a caveat in cases of severe anaemia or carbon monoxide poisoning. Then it is clinically appropriate for the highest concentration of oxygen to be administered.

Tight circulatory monitoring and support

Inotropic support may also be needed early. A degree of myocardial dysfunction/stunning is expected following CPR. To ensure adequate cerebral perfusion we need to target an age-specific, physiologically normal blood pressure. Both hypo and hypertension can exacerbate secondary brain injury. Because of this, monitoring the blood pressure through an arterial line is preferred. If the local set-up or skillset does not allow for arterial line placement, especially in smaller children, having non invasive blood pressure on 1-2 minute cycles can be a useful proxy.  

The paediatric myocardium is much more resilient than its adult counterpart.  If the arrest is not secondary to congenital heart disease the paediatric heart can regain normal function within 12-24 hours.  During the first 20 minutes following ROSC poor cardiac function is due to profound systemic vasoconstriction and cellular acidosis. We can support the myocardium by supplying adequate fluid resuscitation, targeting normal (age-appropriate) blood pressure and inotropic support. Point of care ultrasound, CVP monitoring, or assessing for hepatomegaly/rales if there is no access to the former, can help us prevent fluid overload

Inotrope choice is usually made with the help of the critical care team and depends on the balance between the need for inotropy and vasoconstriction.  Adrenaline is preferred for inotropy, noradrenaline for vasoconstriction.  Be aware that severe acidosis can cause catecholamine resistance, so giving some bicarbonate if the pH <7 may help your inotropes work better. Routine administration of bicarbonate has not been shown to improve clinical outcomes. There are some special circumstances in which we should consider its use such as cases of hyperkalaemia or hypermagnesaemia and arrests due to tricyclic antidepressant overdose. 

Patient position

The patient position that can achieve optimum cerebral perfusion is with the patient semi-sat up at a 30-45 degree angle.

Eucapnia and normoventilation

Avoidance of hypercapnia or hypocapnia is important in preventing secondary brain injury. It is, therefore, recommended that eucapnia is achieved by targeting a PaCO2 between 4.5 and 5.5 kPa. Hyperventilation can cause hypoxia and increase intracranial pressure due to hyperaemia, it can also cause further cerebral ischemia. As the intrathoracic pressures increase, cardiac venous return is impaired. Since the myocardium is already injured this can have catastrophic effects causing the BP to plummet and subsequently impair cerebral perfusion.

Vigilant glucose monitoring 

Following ROSC, children are also at risk of developing hypoglycemia (glucose <3 mmol/L). There is good evidence to suggest that hypoglycaemia negatively impacts neurological outcome and cause hypoglycaemic seizures, especially in the younger ages. Vigilant glucose monitoring and correction as per APLS guidelines is important. If regular dextrose boluses are needed, consider a continuous glucose infusion. If the patient mounts an adequate stress response, they may become hyperglycaemic.  There is no evidence to suggest that aggressive glucose control with insulin in the non-diabetic patient is beneficial; wait with watchful deliberation and the glucose will usually return to normal levels with no intervention.

Frequent neurological assessment

It is important to frequently assess neurological status frequently after ROSC as this can help us prognosticate. Take the time to do a very quick assessment ideally before the administration of anaesthetic agents and paralysis. Document clearly pupillary size/reactivity, GCS (and its break down) and any respiratory effort or gasping. 

Adjunctive investigations

Following ROSC a number of investigations will be needed to guide diagnosis and therapy. Routine bloods such as renal function, electrolytes, liver function tests, full blood count, and clotting are a basic standard. In cases of lactaemia and/or severe metabolic acidosis ammonia and toxicology is useful. Arterial blood sampling is invaluable to allow quick correction of any electrolyte abnormalities and help titrate ventilation settings and (in part) guide inotropic support. Arterial samples will also help uncover any exposure to carbon monoxide, especially in burns cases. 

From an imaging perspective, a chest X-ray is vital in ascertaining tube positioning and lung pathology as well as cardiac contours in case a congenital or acquired heart disease is suspected. Head CT is obviously useful in cases in keeping with traumatic arrest and NAI but timing of the CT and whether it should take place pre-departure to PICU or after depends largely on local trauma network protocols so should ideally be discussed with the regional trauma team lead and paediatric critical care transport team. 

Children that die or arrest unexpectedly in the UK are subject to a sudden unexpected death in infancy investigation (SUDI) so the appropriate referrals need to be made to the child protection team, police and social care. It is important to clarify that even near-miss cases merit triggering the same SUDI process to ensure that any NAI cases don’t slip through the net. 

Transport pearls

After ROSC the patients will need stabilisation and transfer to PICU for on-going management. Depending on the geographical location of your hospital and the availability of a critical care retrieval service you may have to transfer the patient yourselves or look after them until he/she is retrieved by transport team. A good transport and adequate neuroprotection can be achieved by applying these simple pearls: 

  1. Aggressive temperature monitoring and control between 33°C and 37°C.
  2. Monitor for seizures and pre-empt with long-acting antiepileptic accordingly.
  3. Correct electrolytes and hypoglycaemia and monitor frequently.
  4. Nurse the patient a 45° degree angle.
  5. Aim for a higher end of normal BP and use inotropes to achieve this. If you can’t insert an arterial line, have the NIVBP cycle every couple of minutes. 
  6. In cases of trauma, blood products should be used for volume. In an atraumatic arrest, balanced solution boluses are less harmful than 0.9% saline; don’t forget that you are still likely to need blood products. 
  7. Aim for a pCO2 of 4.5-5.5 kPa; use your continuous EtCO2 monitor to titrate ventilation. 
  8. Vigilant and through history/examination to rule out NAI. Free up a member of the team to do a thorough history from the family, always suspect NAI until proven otherwise especially in children under 6 months. 
  9. Know your anaesthetic drug side-effects (atropine dilates pupils for example so impairs our ability to monitor for seizures). Primum non nocere. 
  10. Intraosseous access can be used instead of a central line, have a low threshold to insert one and do it early.
  11. Have a member of the team check-in with the family every 10-15 minutes to explain what is happening, this is a bad day at work for you but probably the worst day of their lives. 

Conclusion

Achieving ROSC is an important step to give our patients a shot at survival. In some cases, achieving ROSC can only give us enough time to prognosticate and understand that survival is not possible. In some other cases ROSC can be the stepping-stone for a good, meaningful survival with a good quality of life. To achieve that, we must be able to apply good quality post–ROSC care and aggressive, pre-emptive neuroprotection. Learn the PCAS disease process to beat the PCAS disease process.  The APLS algorithm has become the bread and butter of anyone that is involved in paediatric care. Understanding and applying the principles of post-cardiac arrest syndrome is equally vital in improving survival outcomes for our patients. Learn the pearls, use them, teach them and I guarantee that it will make a difference.

Coaching in Paediatric Resus

Cite this article as:
Andrew Tagg. Coaching in Paediatric Resus, Don't Forget the Bubbles, 2018. Available at:
https://doi.org/10.31440/DFTB.16514

Paediatric resuscitation is, thankfully, a rare event. When it happens we want to take every advantage of the training afforded to us and so we often turn to simulation. Any resuscitation can create a feeling of overwhelm, of cognitive overload, and so it makes some sense to offload some of the tasks of the team leader to someone else – a coach.

Cheng A, Duff JP, Kessler D, Tofil NM, Davidson J, Lin Y, Chatfield J, Brown LL, Hunt EA, Nye M, Gaither S. Optimizing CPR Performance with CPR Coaching for Pediatric Cardiac Arrest: A Randomized Simulation-based Clinical Trial. Resuscitation. 2018 Aug 24.


Population

Paediatric health care providers from either the ICU or the Emergency Department from one of the four hospitals involved. They were recruited into teams of five. These were made up of a team leader, an airway person, 2 CPR providers and either a coach or extra provider depending on study arm.

Intervention

Each group watched a standard orientation video then completed a scenario that included two confederates. They then ran through a standard simulated arrest scenario. The group was made up of leader, airway, 2 providers and a coach.

What is a CPR coach?

The role of coach is an interesting one.  Dr. Betsy Hunt and her team at Johns Hopkins Children’s Centre introduced the concept of a CPR Coach. They stand by the defibrillator and focus on the quality of CPR providing positive reinforcement and encouragement using a number of techniques.

  • Alert team members to CPR feedback device output
  • Provide verbal corrective feedback based on data provided. e.g. press faster, deeper, slower.
  • Reinforce positive performance
  • Coordinate the correct ratio of ventilations to compressions
  • Help reduce peri-procedural pauses in compressions

Comparitor

This was the standard group set up comprised of a team leader, airway person, and 3 bedside CPR providers.

Outcomes

Both groups were run through a complex 18 minute paediatric arrest scenario that progressed from hyperkalemia to pulseless VT then VF and finally to PEA. A CPR feedback device attached to the mannequin and the defibrillator recorded a number of data points.

The primary outcome measure was percentage of overall excellent CPR – defined as appropriate depth AND rate of chest compressions as recommended by the AHA.

The secondary outcome measures included percentage of compressions at the correct depth OR correct rate, the chest compression fraction, the duration of pre-, peri- and post-shock pauses and the mean rate and depth of compressions during each event.

 

 

Before we get carried away let’s take a sceptical look at the methodology. This was a prospective, multicentre, randomized control trial and so I’ll use the BEEM RCT critical appraisal device.

1.The study population included or focused on those in the ED.

It certainly did as participants were drawn from both ICU and ED.

2.The participants were adequately randomized.

Participants were randomized by team rather than by individual and was stratified by site. The authors do not mention how this randomization took place.

3.The randomization process was concealed. 

Unsure

4. The teams were analyzed in the groups to which they were randomized. 

Yes

5. The study groups were recruited consecutively (i.e. no selection bias).

How individuals were actually recruited is not mentioned in the paper. Perhaps these willing volunteers were already pretty confident of their skillset in one institution due to a robust training program and were less confident at an alternate site?

6. The members of both groups were similar with respect to prognostic factors.  

Demographic data is provided in table 1. Statistical significance is not reported for any of the variance between groups so I wondered if this might have an impact on outcome measures. What interested me most was the number of female participants in the coaching group (83%) vs the control group (75%) and the number of instructors in each group (18% in the coached group vs 8% in the controls). At first glance these may look like significant differences but they are not.

7. All participants (patients, clinicians, outcome assessors) were unaware of group allocation.

Clearly all of the participants knew if there was a coach in the group. Given that outcome assessment was performed by a machine it is unlikely that it knew.

8. Both groups were treated equally except for the intervention.

CPR coaches received an hour of individual extra training. Given that the focus of this training – on the quality of CPR – was not provided to the control groups then it is possible that they would be less focussed on outcomes. There is also the potential that coaches could have spoken to their teams regarding the training they received given that it was provided up to 48 hours prior to the assessment session.

9. Follow-up was complete (i.e. at least 80% for both groups).

Yes.

10. All patient-important outcomes were considered. 

This is a simulation study and, as such, can only really tell us how good the team is at trying to bring a piece of plastic back to life. The group have previously looked at translation of simulated practice into real life scenarios.

11. The treatment effect was large enough and precise enough to be clinically significant.

With regard to the primary outcome measure the coached team performed much better than the control group – 63.3% (53.3 – 73.3) excellent CPR compared with 31.5% (21.5-41.5). Breaking down individual elements by looking at the secondary outcome measures there was also a marked improvement across all groups.

 

My thoughts

All in all this was a well done study that makes me think about how I can utilize the role of CPR coach in both my paediatric and adult practice. The coach in this study used a proprietary feedback device that relayed information to the defib/monitor about both rate and depth of compressions. Is the role still a valid one if such information is not available? Running a paediatric arrest can be very confronting for all involved and the opportunity to cognitively offload even some of the burden seems tempting. We know that the key tenet of effective resuscitation is performing quality CPR and reducing the time off the chest by minimising pauses in compressions. The data suggests that the coach can reduce these pauses and so might be a valuable role even without the feedback device.

In my experience, whenever there is a paediatric arrest staff miraculously appear from out of the woodwork. Nurses, doctors and social workers appear from all over the hospital to help out and perhaps some of these folk could be trained in the coaching role?

 

 

COI declaration: I had a wonderful morning with Betsy Hunt on here recent Australian tour when she took a small group of us through the technique.

The ideal paediatric resuscitation

Cite this article as:
Ben Lawton. The ideal paediatric resuscitation, Don't Forget the Bubbles, 2017. Available at:
https://doi.org/10.31440/DFTB.11246

The first few minutes of a paediatric resuscitation are intimidating and crucial. Every basic life support update we do drills the DRSABCD mnemonic.

Test yourself - What does DRSABCD stand for?

D – Danger – put on some PPE and think situational awareness.

R – Response – pinch the child’s trapezius while asking them to open their eyes..

S – Shout/Send for help – what is the number to call in your hospital?

A – Airway – open it and look for obstructions

B – Breathing – 2 rescue breaths

C – Compressions – 2:15 ratio with breaths, rate 100-120/min, depth 1/3 of the chest. N.B the two thumb technique is recommended in the current guidelines

D – Défibrillation – 4js/kg, manual defib if you have one, AED with attenuated leads next best, standard AED if no alternative.

The team from Princess Margaret in Perth have made this excellent video of what it ought to look like. Enjoy.

If you want to be able to run a calmer resuscitation come and listen to Tim Horeczko of the Pediatric Emergency Playbook at DFTB17

Mechanical CPR in children

Cite this article as:
Andrew Tagg. Mechanical CPR in children, Don't Forget the Bubbles, 2017. Available at:
https://doi.org/10.31440/DFTB.11177

Sometimes a single tweet can stir up something deep inside me that I want to know the answer to.  This time it was Jim DuCanto, airway guru.

Since this is a blog about paediatrics I won’t go into my opinions about mechanical CPR (mCPR) in grown ups. I’ll leave it to Robbie Simpson to rant for me. I have very limited experience in its use which really leads to opinion based rather than evidence based medicine.

My limited experience

I have been at the airway end when it was used as a bridge to ECMO and the cath lab in a case of VF storm in a man younger than me. He walked out of the hospital neurologically intact (N=1). I have also seen many, many dead – if not for the rhythmic mechanical thumping on the chest – that I have had to pronounce when they get to hospital instead of them being left in their own home/residential facility.

Cardiorespiratory arrests in kids are rare with an incidence of around 1-20 per 100,000 person years. The majority are respiratory or due to progressive circulatory shock and occur when physiological compensation can no longer occur. Other than a few rare instances cardiopulmonary resuscitation is liable to be futile. One large study of paediatric arrests found that of those children transported to hospital by EMS survival to discharge was 7.8% (3.5% of infants, 10.4% of children and 12.6% of adolescents). According to the ROC Epistry – Cardiac Arrest the incidence of a shockable rhythm was 4-5% in infants and 15% in adolescents.

 

Jim posited that mCPR might buy staff breathing room to plan interventions, but the intervention that is most likely to be effective is airway control and ventilation.

Both devices in current use – the Autopulse and LUCAS-2 – specifically mention paediatric arrests as a contraindication to use. And it is easy to see why. With such variability in sizes it would be near impossible to build a machine that could work on every size of child. So is there an alternative?

Perhaps, rather than relying on technology to do our job better we should focus on incremental gains – doing the basics well.

 

Airway

Even in a large Melbourne quaternary paediatric centre endotracheal intubation is a rare event with only 71 reported events over a one year time period. The majority of these were due to trauma or status epilepticus rather than cardiac arrest. Even then, the first pass success rate was 78%. Other studies have shown an even lower incidence of first pass success when video review was used. They also are associated with prolonged pauses in CPR. You might think that using video laryngoscopy might improve things but that doesn’t seem to be the case in simulation based studies.

 

Breathing

Once the tube has gone through the cords we often breath a sigh of relief. If you are anything like me you may have been holding your breath for the attempt and there is a tendency to hyperventilate the patient. A review of simulated paediatric codes found that every single one of them ended up with the patient being bagged around a rate of 40 breaths per minutes rather than the recommended 8-20 breaths. If we want to up our game perhaps we could consider adding an impedance threshold device. These valves attach to the endotracheal tube and limit air entering the lung during the passive expansion phase. This creates a reduction in negative intrathoracic pressure thus improving venous return.

 

Circulation

There still seems to be a fear, amongst some healthcare providers, of inserting an intraosseous needle.  It can be confronting, crunching through the outer cortex of bone, but it can (and should) be completed in seconds.

 

High quality chest compressions

Most studies of paediatric CPR involve small numbers of patients and the heterogenous nature of the circumstances surrounding the arrests make it difficult to combine the data in a meta-analysis. The higher quality studies rely upon video review of the events rather than bystander or scribe feedback. A number of common themes emerge. Chest compressions are performed more slowly than recommended around 10% of the time and too fast around 44% of the time. Once simple low-tech way of improving this is the use of a metronome (or a metronome app if you are so inclined).

We are used to practicing CPR on adult mannequins and know how far to compress the chest. This is less obvious in children and we have a tendency to lean on the chest during the decompression phase. Force transduce/accelerometer technology can provide real time feedback

It’s hard to get real time feedback regarding the quality of compressions and so practitioners could take a leaf from the world of adult resuscitation and use end tidal CO2 as a surrogate marker for perfusion.

Low dose, high frequency training can help staff retain their skills. Rather than mandated tri-yearly refresher courses, brief booster training has been shown to be equally as effective in improving skill retention.

One other effect of technology has not been considered. It is that it removes us from our patients. It distances us at a time when our empathy needs to be at its greatest. When CPR fails (and it will) how will we feel if we had done everything, using a machine to pump on the chest? Would we feel better or worse than if we had laid on hands? Would it make our young patient more of a person, of a life lived, or less, in our eyes?

 

So how can we create a calmer resuscitation? Come to DFTB17 and listen to Tim Horeczko to find out.

References


Atkins DL, Everson-Stewart S, Sears GK, Daya M, Osmond MH, Warden CR, Berg RA, Resuscitation Outcomes Consortium Investigators. Epidemiology and outcomes from out-of-hospital cardiac arrest in children. Circulation. 2009 Mar 24;119(11):1484-91

Leman P, Morley P. Review article: Updated resuscitation guidelines for 2016: A summary of the Australian and New Zealand Committee on Resuscitation recommendations. Emergency Medicine Australasia. 2016 Aug 1;28(4):379-82.

Long E, Sabato S, Babl FE. Endotracheal intubation in the pediatric emergency department. Pediatric Anesthesia. 2014 Dec 1;24(12):1204-11.

Kerrey BT, Rinderknecht AS, Geis GL, Nigrovic LE, Mittiga MR. Rapid sequence intubation for pediatric emergency patients: higher frequency of failed attempts and adverse effects found by video review. Annals of emergency medicine. 2012 Sep 30;60(3):251-9.

Niebauer JM, White ML, Zinkan JL, Youngblood AQ, Tofil NM. Hyperventilation in pediatric resuscitation: performance in simulated pediatric medical emergencies. Pediatrics. 2011 Nov 1;128(5):e1195-200

Schuerner P, Grande B, Piegeler T, Schlaepfer M, Saager L, Hutcherson MT, Spahn DR, Ruetzler K. Hands-off time for endotracheal intubation during CPR is not altered by the use of the C-MAC video-laryngoscope compared to conventional direct laryngoscopy. A randomized crossover manikin study. PloS one. 2016 May 19;11(5):e0155997.

Milander MM, Hiscok PS, Sanders AB, Kern KB, Berg RA, Ewy GA. Chest compression and ventilation rates during cardiopulmonary resuscitation: the effects of audible tone guidance. Academic Emergency Medicine. 1995 Aug 1;2(8):708-13.

Sutton RM, Niles D, Meaney PA, Aplenc R, French B, Abella BS, Lengetti EL, Berg RA, Helfaer MA, Nadkarni V. Low-dose, high-frequency CPR training improves skill retention of in-hospital pediatric providers. Pediatrics. 2011 Jul 1;128(1):e145-51.

Bhende MS, Thompson AE. Evaluation of an end-tidal CO2 detector during pediatric cardiopulmonary resuscitation. Pediatrics. 1995 Mar 1;95(3):395-9.