Chest compressions alternate to abdominal compression–decompression technique


Background
The abdominal compression–decompression technique is based on an “abdominal pump” model, which induces pressure changes within the abdominal cavity and promotes the return of blood from the abdominal cavity to fill the heart and be eventually pumped to the brain. A combination of abdominal compression–decompression and chest compression was previously shown to increase the venous refilling of the heart, which could generate increased coronary perfusion pressure and increase blood flow to vital organs . With this combination method, chest release during abdominal compression leads to increased venous return to the thorax by negative intrathoracic pressure. Moreover, abdominal decompression during chest compression may lead to increased blood flow via decreased afterload. In myocardial blood flow, a better 48-h outcome was documented with the combination method compared with STD-CPR
The study
This study was performed in China. It’s a single center, randomised, not blinded study.
The study aimed to compare the outcomes of standard cardiopulmonary resuscitation (STD- CPR) and combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation (CO-CPR) following out-of-hospital cardiac arrest (OHCA).
Primary outcome ROSC. Secondary outcome hospital admission, hospital discharge and neurological outcome at hospital discharge.
Results
ROSC and survival to hospital admission: no statistical benefit
Survival at hospital discharge and neurological outcome: CO-CPR had statistical significant better outcome respect STD-CPR
Limitations
Single center, small sample size, no evaluation of possible abdominal injuries.
Bottom line
For prehospital use of combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation we have first of all to account the need of an additional rescuer to perform abdominal compression-decompression. By the way the alternate chest/abdominal compression-decompression method is promising even if we need larger multicenter randomised trial for a more consistent evaluation of its efficacy.
Head and thorax elevation during cardiopulmonary resuscitation

Background
Gradual elevation of the head and thorax enhances venous return from the head and neck to the thorax and further lowers intracranial pressure. This automated controlled elevation (ACE) CPR strategy consists of: (1) manual active compression decompression (ACD)-CPR and/or suction cup-based automated (LUCAS 3) CPR; (2) an impedance threshold device (ITD); and (3) an automated controlled head and thorax patient positioning device (APPD).
The study
Observational, prospective study. The Objectives of the study was to assess the probability of OHCA survival to hospital discharge after ACE-CPR versus C-CPR. ACE-CPR data were collected from a dedicated registry implemented by 10 EMS Agencies. Conventional (C) CPR data were collected from 3 large historical randomized controlled OHCA resuscitation trials.
NB: for ACE-CPR only 6/10 agencies data were evaluated.
The primary outcome was survival to hospital discharge. Secondary outcomes included ROSC at any time, and survival to hospital dis- charge with favorable neurological function.
Results
Cumulative results on primary and secondary outcome before taking into consideration the time from 911 call to ACE-CPR were not statistically significative differences. The statistical significance of ACE-CPR was reached only when time from 911 call to ACE-CPR initiation was considered.
Limitations
Observational study. Participating personnel form EMS agencies were highly motivated about ACE-CPR. 165 patients excluded with no clear explanation (generally didn’t meet inclusion criteria) from 4 EMS participating agencies. Statistical significance on primary and secondary outcome was reached after surrogate secondary analysis that considered time form 911 call to ACE-CPR start.
Bottom line
There are still insufficient historical data to understand the benefit of automated controlled elevation (ACE) CPR and this study doesn’t clear any doubt about it’s efficacies on clinical oriented outcomes.
Aortic occlusion during cardiac arrest. Mechanical adrenaline?

Background
Thoracic aortic occlusion during chest compressions limits the vascular bed for the generated cardiac output. This may increase the aortic pressure and subsequently the coronary perfusion pressure (CPP).
The coronary perfusion pressure (CPP), the pressure gradient between the aorta and right atrium, is a major determinant of the myocardial blood flow. Consequently, generating a high CPP by providing high-quality chest compression during CPR is one of the most critical factors for achieving ROSC in cardiac arrest patients.
It is uncontroversial to state that the desired effect of adrenaline in CPR is the potential increase in CPP. The potential detrimental effects of adrenaline, such as decreased cerebral blood flow, increased myocardial oxygen consumption or recurrent ventricular tachycardias after ROSC, is yet to be found with REBOA. However, adverse effects of REBOA are not reported in the limited human data published, nor has this been an endpoint in the studies conducted so far.
The study
This is a pilot study. The aim of the study was to calculate the CPP before and after REBOA balloon inflation. EtCO2 and median aortic pressure before and after balloon inflating were also measured.
Results
CPP, MAP and EtCO2 significative increased after REBOA placement in Zone 1 and balloon inflation
Limitations
Single center, small numbers, need of a large number of operators to insert the REBOA and to obtain the measurements.
Bottom line
REBOA in Cardiac Arrest is potentially useful to increase CPP and less dangerous than epinephrine administration.
It’s feasibility in emergency (in-hospital and out of hospital) settings in a timely manner and with a small number of medical personnel needs to be demonstrated.

Don’t live me Breathless
28 GenCase presentation
You arrive on the scene of a motorbike accident. The driver, a 50 years old male, at your arrival is in “Pain” state with eyes closed and you can hear just a “snoring” sound coming from his mouth. His vitals are: NIMBP 80 over 50, HR 110, A quick primary survey reveal a low level of consciousness (eyes closed no finalised arms movement) with restored airway patency that after basic airway manoeuvres and O2 therapy (SaO2 goes to 95%) no signs of tension pneumo. A quick look to the pelvis and legs reveal a suspected “open book” lesion and a bilateral femoral fracture. No PMH is available at the moment.
Physiological response to shock
From the primary survey and vitals you can understand the patient is compensating a state of profound (hypovolemic) shock and consequent organ low perfusion with a sympathetic activation. Endogenous adrenergic mediators are trying to restore organ perfusion by vasoconstriction and increase in cardiac output.
First do not harm
Can we kill a patient destroying the physiologic response to shock?
The answer is YES! The need to protect airway performing a rapid pharmacological assisted airway management (RSI), can lead to bad consequences, destroying the physiological response to a state of profound shock.
All sedative, analgesic and anaesthetic drugs in fact antagonise and depress the sympathetic adrenergic response physiologically targeted to restore perfusion to vital organs.
First do not harm and choose minimal emodynamic impact type and dose of drugs to perform sedation. As we know (till now) the better choice are Ketamine and Etomidate with no clear evidences on which one is preferable. We for sure know that Ketamine can be dangerous in cathecolamine depleted patients and that this effect is dose dependent. So consider using a lower dose to reach dissociative threshold being conscious that can lead to a non ideal intubation condition.
Reanimate first intubate later (aka DSI)
After a dissociative dose of Ketamine, our next clinical target is to reanimate the patient form an oxygenation and/or an organ perfusion point of view.
So we shift from a concept of Rapid Sequence Intubation to a more comprehensive plan of Delayed Sequence Airway Management. Delayed (Ketamine/Etomidate induced) to get time and reanimate, Airway Management intended as any plan (tracheal intubation, supraglottic airway) we can apply in that specific patient in the middle of the road or in other prehospital scenarios.
A properly performed pre-oxygenation with the adjunct of apneic oxygenation can restore O2 levels giving us also a good reserve for following apnea times.
Cautelative fluid administration (avoid fluids in trauma, use BLOOD) and, push dose (Epinephrine, Phenilephrine) or continuous infusion (Norepinephrine) vasopressors, can restore perfusion to abdominal and extra abdominal organs by increasing circulating volume and cardiac performance (Alfa and Beta agonist ).
Delayed paralytic administration give us the time to perform a proper reanimation reanimation and to check the effects of our interventions.
If everything goes well and the patient’s oxygenation and emodynamic state is compensated, we can administer paralytic, and go straight to perform tracheal intubation.
But if the patient remains uncompensated despite all our efforts to correct the potentially lethal cause, our last weapon can be to preserve spontaneous breathing.
Don’t live me breathless
WHY? During inspiratory phase of respiratory cycle the negative intrathoracic pressure favourites venous return and increase the telediastolic volume of the left ventricle. The augmented left ventricle end diastolic pressure (LVEDP) according to Frank-Starling law improves myocardial performance increasing stroke volume and consequently cardiac output.
The refractory shocked patient is heavily preload dependent and suppressing the inspiratory drive risk to worsen the already dramatic emodynamic state taking him on the irreversible part of the shock curve.
We’ve got a plan
We need to have a plan for high difficult physiological airways. This is just a small residual percentage of the airways we manage in our clinical practice, but can be dramatically catastrophic when we deal with those patients without a precise plan.
We’ve got a backup plan
But when intubation fails we need to have a backup plan!
Case conclusion
You understand the need to protect patient’s airways but also the extreme physiologic difficulty of this airway.
After administering a dissociative dose of Ketamine, due to the failure of any try to restore perfusion, you decide to perform a DISSOCIATIVE INTUBATION using a videolaryngoscope with a hyperangulated blade and a bougie, AVOIDING PARALYSIS.
Then you put the patient on ACV mechanical ventilation targeting a TV of 6 ml/kg and considering a “zero PEEP” strategy.
Special Thanks to Scott Weingart and Jim DuCanto for the kindness and fundamental mentorship on inspiring and peer reviewing the algorithm
References
Brian E. Driver, Matthew E. Prekker, Robert F. Reardon, Benjamin J. Sandefur, Michael D. April, Ron M. Walls, Calvin A. Brown,
Success and Complications of the Ketamine-Only Intubation Method in the Emergency Department,
The Journal of Emergency Medicine
Weingart SD, Trueger NS, Wong N, Scofi J, Singh N, Rudolph SS. Delayed sequence intubation: a prospective observational study. Ann Emerg Med. 2015 Apr;65(4):349-55. doi: 10.1016/j.annemergmed.2014.09.025. Epub 2014 Oct 23. PMID: 25447559.
Merelman AH, Perlmutter MC, Strayer RJ. Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine. West J Emerg Med. 2019 May;20(3):466-471. doi: 10.5811/westjem.2019.4.42753. Epub 2019 Apr 26. PMID: 31123547; PMCID: PMC6526883.
Ko BS, Ahn R, Ryoo SM, et al. Prevalence and outcomes of endotracheal intubation–related cardiac arrest in the ED. Am J Emerg Med. 2015;33(11):1642-5.
Mort TC. Complications of emergency tracheal intubation: hemodynamic alterations – part I. J Intensive Care Med. 2007;22(3):157-65.
Jarvis JL, Gonzales J, Johns D, et al. Implementation of a clinical bundle to reduce out-of-pospital peri-intubation hypoxia. Ann Emerg Med.2018;72(3):272-279.e1.
Roantree RAG, Goldstein S. (2018). EMS, Facilitated Intubation Without 36.Paralytics. Treasure Island, Florida: StatPearls Publishing.
Braude D, Palomo O, Beamsley A. Sedation only intubation. EM:RAP. 39.2013.
Miller M, Kruit N, Heldreich C, et al. Hemodynamic response afterrapid sequence induction with ketamine in out-of-hospital patients 50. at risk of shock as defined by the shock index. Ann Emerg Med. 2016;68(2):181-8.e2.
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