Should we withhold chest compressions in traumatic cardiac arrest. A (very) reasonable poin of view.
Epinephrine in cardiac arrest: the past, the present and the (im)possible future. Reflections after PARAMEDIC 2 trial.
23 Jul
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 
The Present: PARAMEDIC 2 trial.
What kind of study is this:
Randomized, double-blind, multicentric.
Population
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.
Strengths
- Randomized, multicenter, double blind, placebo controlled
- 8014 patients randomised.
- 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 limited to 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
References
- 1900: The discovery of epinephrine (adrenaline)
- Hagihara A, Hasegawa M, et al. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA, March 21, 2012—Vol 307, No. 11
- Clifton W. Callaway, MD, PhD. Questioning the Use of Epinephrine to Treat Cardiac Arrest. JAMA, March 21, 2012—Vol 307, No. 11
- Lin S, et al. Adrenaline for out-of-hospital cardiac arrest resuscitation: A systematic review and meta-analysis of randomized controlled trials. Resuscitation (2014).
- G.D. Perkins, C. Ji, C.D. Deakin, et al.A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. Supplementary Appendix.
- Clifton W. Callaway, M.D., Ph.D and Michael W. Donnino, M.D.Testing Epinephrine for Out-of-Hospital Cardiac Arrest.
-
Rethinking Adrenaline in Cardiac Arrest- Jim Manning on Vimeo from SMACC Dub
- Manning JE, Murphy CA Jr. Aortic arch versus central venous epinephrine during CPR. Ann Emerg Med. 1993 Apr;22(4):703-8.
- Manning Rethinking Adrenaline in Cardiac Arrest
Pseudo PEA? When, How, What?
17 Jul
Clinical Scenario
55 years old male arrested in front of the ACLS team in prehospital setting.
The call was due to hypotension and cold sweeting. The team found the patient conscious and responding to their answers. He denied chest pain or dyspnea, referring just dizziness and profound astenia.
No time to put him on monitor and BOOM! Cardiac arrest occurred. PEA. Narrow organised EKG activity, no carotid pulse no indirect signs of circulation.
Mechanical CPR and standard ACLS started. First rhythm control, probe on the chest (subxifoid view)
HEART IS MOVING! NO CAROTID PULSE YET. This is not a cardiac arrest, but it’s not ROSC either!
What’s this condition? For standard ACLS it doesn’t exists, it’s not mentioned and there are no practice guidelines to follow.
But beyond ACLS this is a well recognised situation and is called PSEUDO PEA.
Pseudo PEA
In a recent trial (Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial link in the references) evaluating the use of POCUS in extreme shock and cardiac arrest in prehospital setting the investigators found that, examining with ultrasound patients in cardiac arrest, 74,5% and 35% of PEA and Asystole respectively had cardiac wall motion and a rate of survival significatively higher than “no cardiac activity patients” (55% vs 8% in PEA and 24% vs 11% in Asystole)
Image attribution How Do You FEEL About Echo in Cardiac Arrest?
Three simple steps to manage pseudo PEA
Let’s go back to the clinical case (just to mention this is not a simulated scenario, the patient was real and the team was not from another part of the planet but was my team) How you manage this patient beyond and in absence of clear guidelines?
- Looking for reversible causes
- Monitoring perfusion
- Supporting circulation
Looking for reversible causes
Searching for reversible causes of PEA is a mix between clinical history, physical exams and instrumental findings. I’m not a great fan of H’s and T’s approach.
I use ultrasound!
If you can find the cause, treat it right away, other ways go to next steps monitoring perfusion and supporting circulation.
Monitoring perfusion
Monitoring perfusion in an arrested (technically but not practically) patient on the field (where you don’t have the chance to insert an arterial line to have invasive determination of arterial blood pressure) is a matter of indirect signs and numbers.
“The digitomer” for sure is the worst way to do it. So forget the central pulse it’s subjective and not reliable, as any BLS provider knows.
EtCO2 and pletismographic waveform of capillary pulse are both crucial elements to decide when stopping (or not stopping) CPR and starting vasopressors.
We alla know almost everything about EtCO2 and its value to show perfusion, so I want just to spend some words on a less famous, and widely underestimated, method of monitoring distal perfusion: capillary pulse waveform. We all have pulse ox, few of us consider it’s waveform at all, and certainly not as indicator of perfusion. But a wide range of recent letterature indicates a good correlation between arterial pressure and capillary pressure.
Below you can see the an analysis of the arterial pressure waveform.
Image attribution University College London (UCL) https://doi.org/10.1017/CBO9781139226394.035
and this below is the waveform recorded from a human photoplethysmogram (in other words the waveform shown from any pulse ox) at the capillary level
Image attribution https://www.sciencedirect.com/science/article/pii/S0960077915001344
We don’t need much of evidences to understand how the two waveforms correlates.
So pulse ox waveform can be used as good estimation of arterial pressure and distal perfusion even if we know its often influenced by artefacts expecially in low flow conditions.
I personally consider the EKG trace also a useful tool. An organised electric activity with narrow complexes at a normal rate is more probable to give a perfusing flow than a bradicardic, wide QRS one.
But let’s go back to practical. Which one is the best method to use in prehospital? I personally use all the information, cause in a difficult setting relying on just one of them is dangerous.
So a pseudo PEA condition with narrow complexes electric activity at a rate above 60 bpm, EtCO2 around 35-40 mmHg a good shaped capillary waveform in absence of chest compressions for me is grant of perfusion.
A non organised or wide complexes low rate ekg trace, low EtCO2 and no capillary waveform is a non perfusing state.
Supporting circulation
What to do in those cases?
In the case of “non perfusing” pseudo PEA, no doubt, you need to continue chest compressions to sustain circulatory state.
In the case of “perfusing” pseudo PEA, use vasopressors.
My favourite way to give them, and the more reliable in prehospital environment, is push dose.
My favorite vasopressor is Epinephrine.
Other acceptable alternative is Phenylephrine.
I don’t believe that administering vasopressors in continuous infusion on the field is a good idea. For me is dangerous and not practical. Most of the times we don’t have volumetric or infusion pump ready available so we are not sure about the exact dose administered easily loosing control of the situation.
But in case you intend to give continuous infusion vasopressors use Norepinephrine.
Conclusions
When you have a pseudo PEA patient, the crucial decision is if the present cardiac activity is perfusing (the brain and the other vital organs or not) even in absence of a palpable carotid central pulse.
To understand how is the perfusion going use EtCO2, waveform pulse oximetry and EKG.
If the signs of perfusion are not good continue with chest compressions
If you have good signs of perfusion start vasopressors to sustain circulation.
Remember: This is not an arrested patient! Needs to be in the hospital ASAP to start ECMO, PCA or other definitive care.
Take home points about pseudo PEA:
- ALWAYS use ultrasound to determine cardiac activity in cardiac arrest patients
- Don’t trust central pulse palpation
- Pseudo PEA is an ultrasound evident cardiac activity without carotid pulse
- Pseudo PEA is a big clinical reality beyond ACLS mantras
- Use ultrasound to look for reversible causes of pseudo PEA.
- Use waveform EtCO2 and waveform Pulse Oximetry to monitor perfusion
- Continue CHEST COMPRESSIONS in pseudo PEA with bad perfusion state indicators:
- Wide bradycardic electric activity
- Low EtCO2 (below 20 mmHg)
- No waveform on Pulse ox
- Use VASOPRESSORS in pseudo PEA with good perfusion state indicators:
- Narrow normofrequent electric activity
- EtCO2 above 35-40
- Good waveform on Pulse ox
References
- Breitkreutz R et al. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial.Resuscitation 2010; 81: 1527-33. PMID: 20801576
- Nina Sviridova, Kenshi Sakai, Human photoplethysmogram: new insight into chaotic characteristics,Chaos, Solitons & Fractals, Volume 77, 2015, Pages 53-63,
ISSN 0960-0779, https://doi.org/10.1016/j.chaos.2015.05.005 (http://www.sciencedirect.com/science/article/pii/S0960077915001344) - Section 3: Cardiovascular physiology Chapter 33 Arterial pressure waveforms
Still not time! But we’re moving forward!
12 Jun
We launched several days ago the pool about which was the first choice when dealing with airways in a critical hill patient. Provocatively the pool was introduced by an announcement about the death of Direct Laringoscopy and the rising of Video Laryngoscopy as first choice.
Here are the results!
So it’s stil not time? Yes, but we are moving toward an era where videolaryngoscopy will be the first choice.
Almost one third of the providers are already choosing video as the first choice in environments, prehospital, ER an critical care where this technology is still not widely available and where the classical airway management teaching is still dominated by direct laringoscopy.
My personale thought is that direct laryngoscopy has to be part of the cultural and technical baggage of an emergency provider and has to be part of teaching courses but just as prelude to a clinical practice environment where technology and well trained professionals permit to use the best available device.
Prehospital Emergency Medicine. We are different.
12 May
YES prehospital professionals are different from any other medical provider.
YES Prehospital Emergency Medicine is different because is not just clinical competence and technical skills. It’s much more.
WE are different because performing skills or procedures depends not just from the right patient and the right indication, but is heavily influenced by the environment where we work and the team we lead.
BUT despite this we perform complex procedures even in the hardest situations.
WE are different because we always deal with the “contro” of a possible failure in the middle of nowhere, and the “pro” of a probable success in a safe and warm environment (as the nearest emergency room).
BUT despite this we act, succeed and learn from our failures.
WE are lucky because often our patients don’t have life treating conditions, they just need to talk and we probably are their last chance.
WE love our job.
WE love Prehospital Emergency Medicine.
Join us in Rome to share the same passion
La gestione del paziente critico in emergenza territoriale. Il corso.
8 May
Ci siamo! Manca pochissimo e noi siamo prontissimi ad accogliervi.
Federica Stella, Giacomo Magagnotti, Francesco Patrone ed io Mario Rugna saremo lieti di guidarvi attraverso l’affascinante mondo dell’emergenza territoriale.
Grazie a SIMEU abbiamo creato una faculty formata da professionisti sanitari provenienti dall’emergenza territoriale per un corso completamente dedicato alla gestione extraospedaliera del paziente critico.
Parleremo di gestione dell’arresto cardiaco, di gestione delle vie aeree di diagnosi e terapia delle maggiori emergenze extraospedlaiera attraverso la simulazione ad alta fedeltà e con l’utilizzo di modelli biologici.
Saranno due giorni intensi, interattivi e speriamo divertenti.
Per iscriversi andate sul sito del Congresso SIMEU 2018
Vi aspettiamo!
Articles at the Top. Take home messages from 2017 (part 3). Trauma.
1 MayWelcome to our review of the best articles from the last year.
This will be a weekly (or so..) appointment with the top articles from 2017 divided by topic and chosen by me.
Here is the best about:
Trauma
Traumatic Cardiac Arrest
- Defining the Limits of Resuscitative Emergency Department Thoracotomy: A Contemporary Western Trauma Association Perspective
- Out of Hospital Thoracotomy for Cardiac Arrest after Penetrating Thoracic Trauma
- Revisiting traumatic cardiac arrest: should CPR be initiated?
- Predicting outcomes in traumatic out-of-hospital cardiac arrest: the relevance of Utstein factors
Fluid Therapy
- Does Administration of Hypertonic Solutions Improve Mortality in Hemorrhagic Shock Compared With Isotonic Solutions?
- The effectiveness of prehospital hypertonic saline for hypotensive trauma patients: a systematic review and meta-analysis
- Fluid resuscitation of trauma patients: How much fluid is enough to determine the
patient’s response? - Strategies for Intravenous Fluid Resuscitation in Trauma Patients
- Damage control resuscitation in patients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma
Spinal Immobilisation
- Placement of a cervical collar increases the optic nerve sheath diameter in healthy adults
- Increase in intracranial pressure by application of a rigid cervical collar: a pilot study in healthy volunteers
- Does the novel lateral trauma position cause more motion in an unstable cervical spine injury than the logroll maneuver?
- Value of prehospital assessment of spine fracture by paramedics
- Effects of spinal immobilization at a 20° angle on cerebral oxygen saturations
measured by INVOS
Field Triage
- Accuracy of Prehospital Triage in Selecting Severely Injured Trauma Patients
- The prospective validation of the Modified Physiological Triage Tool (MPTT): an evidence-based approach to major incident triage
- Undertriage Remains a Vexing Problem for Even the Most Highly Developed Trauma Systems The Need for Innovations in Field Triage
- Value of prehospital assessment of spine fracture by paramedics
- Association of Prehospital Mode of Transport With Mortality in Penetrating Trauma
- Association between seatbelt sign and internal injuries in the contemporary airbag era: A retrospective cohort study
- The Reliability of the Pre-hospital Physical Examination of the Pelvis: A Retrospective, Multicenter Study
- Clinical Judgment Is Not Reliable for Reducing Whole-body Computed Tomography Scanning after Isolated High-energy Blunt Trauma
Antifibrinolytics
- Effect of treatment delay on the effectiveness and safety of antifibrinolytics in acute severe haemorrhage: a meta-analysis of individual patient-level data from 40138 bleeding patients
- Tranexamic acid: is it about time?
- Effectiveness of early administration of tranexamic acid in patients with severe trauma
- The effect of tranexamic acid in traumatic brain injury: A randomized controlled
trial
Prehospital blood
- Prehospital Blood Transfusion for Combat Casualties
- Association of Prehospital Blood Product Transfusion During Medical Evacuation of Combat Casualties in Afghanistan With Acute and 30-Day Survival
- Pre-hospital transfusion of packed red blood cells in 147 patients from a UK helicopter emergency medical service
- Pre Hospital Administration of Freeze Dried Plasma, is it the solution for Trauma Casualties?
Massive transfusion protocol
- Every minute counts: Time to delivery of initial massive transfusion cooler and its impact on mortality
- Massive transfusion: An update for the anesthesiologist
Traumatic Brain Injury
- Meta-Analysis of Therapeutic Hypothermia for Traumatic Brain Injury in Adult and Pediatric Patients
- The effect of tranexamic acid in traumatic brain injury- A randomized controlled trial
- Hypothermia for severe traumatic brain injury in adults: Recent lessons from randomized controlled trials
- Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension
- Temporising Extradural Haematoma by Craniostomy Using an Intraosseous Needle
- Coagulopathy in the Setting of Mild Traumatic Brain Injury: Truths and Consequences
- A State-of-the-Science Overview of Randomized Controlled Trials Evaluating Acute Management of Moderate-to-Severe Traumatic Brain Injury
The rest
- Global lessons: developing military trauma care and lessons for civilian practice
- Measurement of blood lactate, D-dimer, and activated prothrombin time improves prediction of in-hospital mortality in adults blunt trauma
- One hundred years on: Ypres and ATLS
- Multiple Trauma and Emergency Room Management
- Research questions in pre-hospital trauma care
- Pre-hospital finger Thoracostomy in Patients with chest trauma
- ‘Major trauma’- now two separate diseases
- DATA CAPTURE AND COMMUNICATION DURING TRANSFERS TO DEFINITIVE CARE IN AN INCLUSIVE TRAUMA SYSTEM
- Vasopressors: Do they have any role in hemorrhagic shock
- Chest wall thickness and decompression failure- A systematic review and meta-analysis comparing anatomic locations in needle thoracostomy
If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.
Don’t kill your patient with a probe! Welcome to UltraSound in Cardiac Arrest for (not so) Dummies!
8 Mar
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.
WHEN we 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.
WHERE we 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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Social media & aggiornamento. Dacci il tuo parere!
18 OctMedici e infermieri d’emergenza-urgenza e area critica, come usate i #SocialMedia per aggiornarvi?
Rispondi a questa breve survey ➡️ bit.ly/2yiVXXI ⬅️per contribuire a delineare la realta’ italiana #FOAMed #FOANed #FOAMcc #AreaCritica #Emergenza
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