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
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).
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.
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.
Personal Protective Equipment for Advanced Life Support interventions need to be at maximum level of protection of full body, eyes and airways.
CAT 3 level of protection 4 (at least) for the full body
FPP2/N95 airway filter for team members who are NOT directly involved in airway management, ventilation or manual chest compressions
FPP3/N99 airway filter for providers who are directly involved in airway management, ventilation and manual chest compressions.
Face shield and protective googles are strongly suggested
Mechanical Chest compressors devices are the gold standard to perform cardiac massage. They reduce contacts and contamination risk and team member exposure to contaminants.
Adhesive disposable pads are the only option to check rhythm and deliver shock. Dispose non-disposable, manual pads.
Passive O2 administration (via simple face mack at a rate of 15l/m) during chest compressions is the first option over bag mask ventilation when performing Basic Life Support waiting for advanced airway management.When using a Bag Valve Mask always put a HEPA/HME filter between Bag and mask to avoid contamination
Hold chest compressions when performing airway managment
Cover patient head with a transparent plastic foil to minimise virus spreading and contamination when performing airway management and bag mask ventilation
Tracheal intubation using a video laryngoscope is the first line option for advanced airway management to minimise contamination.
If video laryngoscope is not available Extraglottic devices are an acceptable first line option
Use all the implementation to improve intubation first passage success:
Video laringoscopy
Bougie
RAMP positioning
Suctioning (SALAD technique)
Use all the implementation to improve Extraglottic device placement
Laryngoscope for tongue displacement and mouth opening (DO NOT USE hands)
Deflate cuff
Lubrificate the device
Whatever plan you apply use an HEPA/HME filter immediately after the ventilation device
Use disposable cover and disposable gel to perform Ultrasound during chest compressions
The past (a brief history of epinephrine use in cardiac arrest)
In 1901 Jokichi Takamine (1854-1922) isolated the pure form of adrenaline, also known as epinephrine.
Routine use of adrenaline for cardiac arrest was first proposed in the 1960’s. Its inclusion within cardiac arrest management was based upon an understanding of the physiological role of adrenaline, and experimental data from animal research which showed that ROSC was more likely when the drug was used.
Epinephrine was not included in cardiac arrest protocols on the basis of evidence of benefit in humans.
Epinephrine remained, since today, a significant component of advanced life support despite minimal human data indicating beneficial effect .
The rationale for use of epinephrine in cardiac arrest was that, in animal studies, increases aortic blood pressure and thus coronary perfusion pressure during chest compressions.
IMPORTANT, brief reminder on epinephrine effect and Coronary Perfusion Pressure.
Coronary vessels are contained in epicardium and their flow is possible in the diastole when they are not compressed by myocardium during systolic contraction.
Coronary flow depends from the gradient between aortic diastolic (Ao) pressure and diastolic left ventricular (LV) pressure.
Higher is the coronary pressure perfusion (CPP), greater is the chance of ROSC.
Epinephrine is a key determinant factor in maintaining diastolic aortic pressure in cardiac arrest; thanks to its interaction with alpha receptors, located on the endothelium of the arteries, produce generalized peripheral arterial vasoconstriction maintaining aortic diastolic pressure to a high level even during chest compressions.
The cut off value for ROSC is 15 mmHg of CPP, but more is better (at least 40 mmHg9.
Many and strong recent evidences demonstrates that “Among patients with OHCA, use of prehospital epinephrine was significantly associated with increased chance of return of spontaneous circulation before hospital arrival but decreased chance of survival and good functional outcomes
8014 patients with out-of-hospital cardiac arrest in the United Kingdom
Inclusion Criteria
Adult (>16 years) patients, transported by five National Health Service ambulance services in the United Kingdom, who had sustained an out-of-hospital cardiac arrest for which advanced life support was provided by trial-trained paramedics.
Exclusion criteria
Apparent pregnancy, age of less than 16 years, cardiac arrest from anaphylaxis or asthma, administration of epinephrine before the arrival of the trial-trained paramedic.
Intervention
Paramedics administered either IV epinephrine 1mg every 3 – 5min + standard care or IV 0.9% normal saline bolus + standard care.
Comparison
Placebo (IV 0.9% normal saline bolus) + standard care
Outcome
Primary outcome:
Rate of survival at 30 days.
Secondary outcomes:
Rate of survival until hospital discharge with a favorable neurologic outcome, as indicated by a score of 3 or less on the modified Rankin scale.
Lengths of stay in the hospital and in the intensive care unit
Rates of survival at hospital discharge and at 3 months
Neurologic outcomes at hospital discharge and at 3 months
Results
Patients who received epinephrine had a higher rate of 30-day survival than those who received placebo.
No clear improvement in functional recovery among the survivors in the epinephrine group.
The proportion of survivors with severe neurologic impairment was higher in the epinephrine group (31.0% vs. 17.8%)
Epinephrine NNT of 112 patients to prevent 1 death at 30-days (Early defibrillation NNT = 5, CPR performed by a bystander NNT = 15 )
Image attribution: REBEL Cast Ep56 – PARAMEDIC-2: Time to Abandon Epinephrine in OHCA?
Conclusions
In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.
Well balanced characteristics at baseline of the two groups
Concurrent treatments were similar
Median time from the emergency call to ambulance arrival was 6.6 minutes
Patient oriented outcomes
Limitations
Overall survival rate in this trial was disappointingly small (3.2% and 2.4%, respectively)
615 patients where excluded because had return of spontaneous circulation before paramedics can open the trial pack. Of these 615 patients of which we don’t know the clinical outcome but including the survivors overall survival rate is similar to other EMS in Europe.
Median time from the emergency call until administration of the trial agent 21 min and we know (according the other studies) that cardiac arrest has 3 phases (Electrical Phase, first 5 min (Defib), Circulatory Phase next 10 – 15min (Chest compressions), Metabolic Phase 10-20min) and epinephrin is effective if administered in the first 20 min of the cardiac arrest.
Information about the quality of CPR was limitedto the first 5 minutes of cardiac arrest and involved <5% of enrolled patients
The protocol neither controlled nor measured in-hospital treatments and we know that the most common cause of in-hospital death is iatrogenic limitation of life support, which may result in the death of potentially viable patients.
What we know till today
Epinephrine in cardiac arrest improve ROSC and patients alive.
The improved survival is mostly due to patients with bad (<3 MRS) neurological outcome.
What that means
Administering the current recommended dose of Epinephrine we have to choose between numbers and quality of life.
Patients clearly said quality of life is more important
Epinephrine is anyway important because having bigger numbers of ROSC give the chance to improve neurological outcomes.
Future challenges
Understanding why epinephrine doesn’t work and can be detrimental on long term neurological outcome.
Obtaining more ROSC and better neurological outcomes in Cardiac Arrest
The (im)possible future
I think there are two key factors, in the actual way to use Epinephrine, that determine its failure:
The wrong administration route
When epinephrine is administered intravenously in a low flow state patient (as is a patient during cardiac arrest, even if proper chest compressions are performed), the amount of drug that arrives to perform the “local” alpha effect on arteries is just a minimal quantity of the (high!!!) dose. The major part rely in the venous circulation and is mobilized in great quantity only when ROSC happens determining a widespread vasoconstriction and a consequent “overdose” effect (think just at the “stunned” myocardium that has to overwhelm such ha great post-load work).
The wrong dose to the wrong patient
From the coronary perfusion pressure (CPP) point of view, every cardiac arrest patient is different: some patients have a (relative) good aortic pressure and a (relative) good coronary perfusione comparing to others.
When we administer the same amount of epinephrine to each of them this takes to an underdose in some patients (with low flow state) and an overdose in others (with good or high flow state).
So now what?
The right administration route
Probably the best route to administer epinephrine is not the vein but the artery.
It allows, even in a low flow state patient, a better chance to reach the vasoconstrictor effect maintaining a good aortic diastolic pressure and a consequent good coronary flow.
The right dose to the right patient
Giving epinephrine (standard dose) to a patient who has a low flow state (patients who need it more) make epinephrine usefulness (underdose) because just a little part of it circulate.
Giving epinephrine to patients in a good or high flow state (patients that need it less or don’t need epi at all) is detrimental and can cause overdose effect.
We need to know wich is the circulatory state of the patients to administer the right dose avoiding the “overdose” effect.
The only way to do this is monitoring aortic diastolic pressure through an arterial catheter. We can target Epinephrine dosage to reach a good aortic pressure maintaining a good CPP (achieving ROSC) and avoiding overdose.
Take home messages for future improvements in cardiac arrest management
Obtain an arterial line
Give Adrenaline intrarterially
Check blood pressure via arterial line
Target Adrenaline (doses and times) to maintain at least 40 mmHg of diastolic arterial pressure
A 2017 study about US and cardiac arrest aroused the debate about using POCUS during cardiac arrest . The authors concluded that:
“The use of POCUS during cardiac arrest resuscitation was associated with significantly increased duration of pulse checks, nearly doubling the 10-s maximum duration recommended in current guidelines.”
THE QUESTION
Is POCUS an unuseful loose of time and a potential KILLER when used on patients in Cardiac Arrest?
In my personal experience (and in the EMS where I work) we tried to give an answer to this question formulating a structured approach to use ultrasound during a code. The objective is to have vital information from the probe without delays or interruption in chest compressions.
THE RATIONALE
In WHICH cardiac arrest using POCUS really worths the price?
For sure PEA and Asistoly are the the most relevant conditions to use a probe, on the contrary in defibrillating rhythms, defibrillation and anti-arythmic therapy is a priority, and no useful information can come from ultrasound.
So look at the monitor, if there is a defibrillating rhythm continue with classical ALS approach.
Use a probe only if Asystoly or a PEA are present.
WHENwe use the probe?
The right moment is during the 10 seconds pause indicated from guidelines to asses the rhythm.
Look at the monitor screen for rhythm check and place the probe on the patient for no longer than 10 seconds.
WHEREwe place the probe.
SubCOSTAL view of the heart for heart beating
SubCOSTAL view of the heart pericardial effusion and VD>VS
Left CHEST view for lung sliding
Right CHEST view for lung slinging
WHAT we can identify with ultrasound during Cardiac Arrest.
First thing is there any cardiac activity?
We no more check the pulse, but rely on indirect signs of cardiac arrest when starting chest compressions, but at the beginning of the code and during the reanimation, cardiac activity is a game changing information.
Second thing is does exists any reversible cause of Cardiac Arrest?
Addressing and treating those can really change the outcome of the patient.
Pulmonary Embolism
Cardiac Tamponade
Tension Pneumo
Hypovolemia
The method
During the 10 sec pause asses the rhythm and place the probe .
During the following 2 min CPR think and address, when indicated, the reversible causes.
THE SCHEDULE
HEART BEATING
If heart is beating and the rhythm is Asystoly think to an equipment problem or to a very fine VF.
If the heart is beating and we have a PEA this is not a true PEA but a pseudo PEA so we have to treat this patient as a profound shock patient (POCUS differential diagnosis for shock) more than CA patient.
If heart is not beating, any rhythm, we look for reversible cause of CA.
PERICARDIAL EFFUSION
VD>VS
If pericardial effusion is present think at CARDIAC TAMPONADE
If VD>VS think at PULMONARY EMBOLISM
If no one of that are present go to the following step
Lung Sliding
If lung sliding is absent think at a selective intubation of the right main bronchus or at a PNX. If lung sliding is present go to the following step.
Lung Sliding
If lung sliding is absent think at a PNX.
Can we scan more during 2 min CPR?
Left flank and look for free fluid.
Right flank and look for free fluid.
If there is free fluid in the abdomen think and treat HYPOVOLEMIA.
REMEMBER! At any time during the code, if EtCO2 rises or a coordinated electric activity is present
NO PULSE CHECK
USE ULTRASOUND TO IDENTIFY A BEATING HEART
TRUST THE PROBE NOT YOUR FINGERS
If no reversible cause are detected, and the patient is still in non defibrillating rhythm, check the heart and the EtCO2.
If heart is not beating and EtCO2 level is less than 10 mmHg. during good quality chest compressions, consider to call the code.
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Learning everything I can from everywhere I can. This is my little blog to keep track of new things medical, paramedical and pre-hospital from a student's perspective.
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MEDEST 
Beyond Guidelines: what’s new in OCHA management
6 SetChest 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
Evaluation of abdominal compression– decompression combined with chest compression CP9R performed by a new device: Is the prognosis improved after this combination CPR technique?
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
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
Head and thorax elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival
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
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
Resuscitative endovascular occlusion of the aorta (REBOA) as a mechanical method for increasing the coronary perfusion pressure in non-traumatic out-of-hospital cardiac arrest patients
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
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