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.
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 dedicatoalla gestione extraospedaliera del paziente critico.
Parleremo di gestione dell’arresto cardiaco, di gestione delle vie aeree di diagnosi e terapia delle maggiori emergenze extraospedlaieraattraverso la simulazione ad alta fedeltà e con l’utilizzo di modelli biologici.
Saranno due giorni intensi, interattivi e speriamo divertenti.
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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.
Yesterday the usual MEDEST letterature review was almost fully pointed on Morphine use in ACS. The cited articles talked about Morphine use and survival outcome or P2Y12 inhibitors absorption. The latest evidence pointed toward less survival and less PY12 absorption when Morphine is administered in patients that suffered of ACS.
First evidences about those effects can be dated to CRUSADE(1) study, but more recently other studies pointed in this direction (2,3, 4).
And what about using Fentanyl instead? Some authors compared Morphine to Fentanyl (4) finding no evidences about the superiority of one on another, and on a recent study (5) Fentanyl carried the same detrimental effect on Ticagrelor absorption.
So we really have to ban Morphine or Opiates in ACS?
In an interesting post (6) Rory Spiegel questioned about the basic assumption that P2Y12 benefits in ACS was never really proven and so, even if P2Y12 inhibition by Morphine was real, no damages derived from Opiates effects on them.
On the other hand Vince di Giulio on EMS 12 leads (7) criticised the methodology of most studies at the basis of the P2Y12 inhibition and detrimental effect on survival.
Are you enough confused? What you really do and what all of this matter for daily clinical practice?
In the meantime you decide this is my personal clinical behaviour on opiates and ACS.
In general I limit Opiates use in ACS only when pain is really a problem for patients(VNS>7) and it was not relieved by NTS.
I’m more concerned about emodynamic profile of opiates so I prefer Fentanyl over Morphine cause is more stable, has a better pharmacological profile and induce less histamine release.
Read more about this topic. Explore the References:
Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM, Peacock WF, Pollack CV Jr, Gibler WB, Peterson ED; CRUSADE Investigators. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005 Jun;149(6):1043-9. doi: 10.1016/j.ahj.2005.02.010. PMID: 15976786.
Parodi G et al. Morphine is Associated with a Delayed Activity of Oral Antiplatelet Agents in Patients with ST-Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circ Cardiovasc Interv. 2014. PMID: 25552565
Puymirat E et al. Correlates of Pre-Hospital Morphine Use in ST-Elevation Myocardial Infartion Patients and its Association with In-Hospital Outcomes and Long-Term Mortality: The FAST-MI (French Registry of Acute ST-Hobl EL et al. Morphine Interaction with Prasugrel: A Double-Blind Cross-Over Trial in Healthy Volunteers. Clin Res Cardiol. 2016. PMCID: PMC4805697Elevation and Non-ST-Elevation Myocardial Infarction) Programme. Eur Heart J 2016. PMID: 26578201
Hobl EL et al. Morphine Interaction with Prasugrel: A Double-Blind Cross-Over Trial in Healthy Volunteers. Clin Res Cardiol. 2016. PMCID: PMC4805697
McEvoy JW, Ibrahim K, Kickler TS, Clarke WA, Hasan RK, Czarny MJ, Keramati AR, Goli RR, Gratton TP, Brinker JA, Chacko M, Hwang CW, Johnston PV, Miller JM, Trost JC, Herzog WR, Blumenthal RS, Thiemann DR, Resar JR, Schulman SP. Effect of Intravenous Fentanyl on Ticagrelor Absorption and Platelet Inhibition Among Patients Undergoing Percutaneous Coronary Intervention: The PACIFY Randomized Clinical Trial. Circulation. 2018 Jan 16;137(3):307-309. Epub 2017 Oct 18. doi: 10.1161/CIRCULATIONAHA.117.031678. PMID: 29046319.
Weldon ER et al. Comparison of Fentanyl and Morphine in the Prehospital Treatment of Ischemic Type Chest Pain. Prehosp Emerg Care 2016. PMID: 26727338
Pathophysiological bases in experimental swine models
In a swine model following primary cardiac arrest the respiration continues at least for 1 minute. and after that Gasping starts lasting for another minute.
In a swine model following primary cardiac arrest the blood shifts from high pressure compartment (arteries) to low pressure compartment (veins).
In a swine model the PaO2 following primary cardiac untreated VF arrests PaO2 results 70 mmHg after 9 min with a saturation of 93% and decrease at 44 mmHg with a saturation of 61% after 14 min of CPR. In this period airway management with possible interruption of chest compressions and starting positive pressure ventilation (with decreased return to the thorax end depression of cardiac output) is not mandatory due to the low cost/beneficial ratio and the potential detrimental effect.
Chest compressions
Chest compressione only CPR is associated with worst outcome in childrenunder 8 yers. Always perform chest compression/ventilation (ratio 15:2) in children <8 years of age (only exception if the cardiac arrest is due to primitive cardiac causes).
Chest compressione only CPR can be a valuable option in adult witnessed VF/pulseless VT primary cardiac arrest (delayed airway management and passive O2 administration is reasonable).
Mechanical chest compression (MCC) is the future of CPR. They still do not demonstrated evident superiority in terms of outcome respect to manual chest compressions, but are evidently not inferior with a similar rate of life treating lesions. For sure MCC avoid variability in quality and allows good quality CC during transport.
Ventilation
Lower Tidal volumes following OHCA is independently associated with favourableneurocognitive outcome
Weak evidences demonstrate that the ideal rate for ventilation of intubated patients during CPR is 10/min
Airway management
There is not beneficial effect on outcome with early intubation in Cardiac Arrest (CA).
Privilege High Quality CPR and Defibrillation (if needed).
Use Supraglottic Airway Devices (SAD) in first part (15 min) of resuscitation
If Mechanical Chest Compressions is used, to optimise ventilation with SAD, use 30:2 ratio (because the intrathoracic pressure generated during MCC overrules that generated from SAD and impaires ventilation).
In prolonged Cardiac Arrest management converting SAD to Endotracheal Tube can be considered.
Experience provider only can perform endotracheal intubation in CA. They have a better chance of first passage rate, without interruption in chest compressions. First pass success rate is positively associated to survival and good neurological outcome.
Defibrillation
Escalating bilevel energy (150-200-360 Joule) is associated with more efficacy in termination of shock resistant VF/pulselessVT cardiac arrest
Dual Sequential Defibrillation is feasible and safe. Although the evidences on its beneficial effect on outcome are still lacking it has to be considered in case of CA with refractory shockable rhythm.
Antiarrhythmics drugs
There has been no conclusive evidence that any antiarrhythmic agents improve rates of ROSC, survival to admission, survival to discharge or neurological outcomes.
Ultrasound
Ultrasound in PEA is a key tool to detect CA causes improving survivival.
Post Resuscitation Care
In post resuscitation phase avoid any arterial oxygen and carbon dioxide abnormality because are associated to increased mortality.
Centralisation of resuscitated patients toward an acute PCI/CABG capable Center is associated to better outcome.
Targeted Temperature Management
Prehospital cooling does not improve faster in-hospital target temperature achieving and due to its costs is not recommended.
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Risk factors for intubation related cardiac arrest are: overweight or obesity, age more than 75 years old, low SBP prior to intubation, hypoxemia prior to intubation, and absence of preoxygenation before intubation procedure.
Preoxygenation is crucial (at least 2 minutes), before paralysing, to extend safe apnea time.
Use apneic oxygenation during intubation attempts.
Tracheal intubation is good in the hands of very well skilled professionals. Otherwise can improve mortality rate.
Supraglottic devices perform well in cardiac arrest and are a valuable option for airway management.
Videolaryngoscopy improve glottic view but need training to improve first pass success.
Always use paralytics when intubating a non cardiac arrest patient. It improves the chances fo first pass success.
Rocuronium and Succynocholine are both valuable options for paralysis in airway management.
Dose Succynocholine, and other depolarising neuromuscular blockade drugs, based on actual body weight. Dose Rocuronium or Vecuronium based on ideal body weight.
Use cuffed tracheal tubes even in paediatric patients. They perform well and complications rate is the same.
The difficult airway is a myth. It’s not a matter of technique but of decision making.
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The objective of chest compressions in CPR is to compress the heart and in particular the Left Ventricle (LV) to generate a stroke volume (SV) trough the Left Ventricular Outflow Tract (LVOT) to perfuse the heart the brain and the rest of the organs.
Performing CPR we blindly compress the center of the chest on the sternum approximately at the level of intermammillar line (as recommended by the 2015 CPR Guidelines) but we risk to apply the Area of Maximum Compression (AMC) not only on the LV but also on the Aortic Valve (AV) and the Ascending Aorta (AA) closing them and generating less (or none) LV stroke volume but just an ineffective retrograde flow.
Image Attribution: Nestaas et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2016) 24:54. Radiological assessment of chest compression point and achievable compression depth in cardiac patients.
Depending on how much the AMC is positioned on the left ventricle or on the aortic part of the heart chest compressions are respectively more or less efficacious to perfuse the brain the heart and the organs.
This is not just theory but was demonstrated in animal and human studies (See References links at the bottom).
In particular Sung Oh Hwang and coll. in the article “Compression of the Left Ventricular Outflow Tract During Cardiopulmonary Resuscitation” observe that”the magnitude of compression of the left ventricle is more significant when a maximal compression occurs at the LVOT than when a maximal compression occurs at the ascending aorta during external chest compression“. They also determined “that external chest compression at the hand position currently recommended by the AHA guidelines compresses the LVOT or the ascending aorta.” and conclude that “(….) the compression location currently recommended by the AHA guidelines may not be effective in generating forward blood flow during CPR.”(….) it is possible that compressing the caudal part of the sternum will improve the quality of CPR and reduce rescuer fatigue.“
The investigators stated also that the Optimal Compression Point (OCP) cannot be definitively addressed because it depends on many variables and varies from patient to patient depending “on the configuration of the heart in the thorax.”
All those findings were assessed using Trans Esophageal Echocardiography (TEE) inserted during CPR in real cases scenarios to visualise the heart to measure the LV stroke volume in order to find the best OCP.
TEE in fact is a good method to study proposition but in a short future will be a good clinical instrument to individually and visually assess the OCP, to deliver biphasic shock and to pace the heart. It is of rapid insertion in the intubated patients, is remotely and in real time monitorizza from team leader doesn’t implicate chest compressions interruption and is safe.
In another study based on a real case series “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography” published in 2013, Eric Qvigstad and coll. found “that the chest compression point generating the highest EtCO2 value was evenly distributed between the patients, indicate that there is no common optimal chest com-pression point within the area tested.”
Image attribution: Qvigstad E, et al. Clinical pilot study of different hand positions during manual chest compressions monitored with capnography. Resuscitation (2013), http://dx.doi.org/10.1016/j.resuscitation.2013.03.010
They individually chosen the best hand position during chest compressions on the basis of EtCO2 values.
So which are the clinical implications for our current clinical practice?
I would like to divide the clinical take home points in two different categories:
Actual applications
Future development
Actual applications for clinical practice
The recommended chest compression point can be ineffective to generate enough outflow because the Area of Maximum Compression is not on the Left Ventricle but either on the Aortic Valve or the Ascending tract of the Aorta
Emergency providers can adjust the compression point based on EtCO2 values.
If, despite technically correct chest compressions, the EtCO2 remains below 10, try to adjust the compression point.
In those cases, the Optimal Compression Point is usually positioned caudally to the recommended one on the lower third of the sternum
Future development for clinical practice
TEE is a clinical useful instrument to
individually and visually assess the OCP
deliver biphasic shock
pace the heart
TEE is of rapid insertion in the intubated patients, can be remotely and in real time controlled from team leader, doesn’t implicate chest compressions interruption and is safe.
Our goal is to inform the global EM community with timely and high yield content about what providers like YOU are seeing and doing everyday in your local ED.
این سایت را به آن دکتوران و محصلین طب که شب و روز برای رفاه نوع انسان فداکاری می کنند ، جوانی و لذایذ زندگی را بدون چشمداشت به امتیاز و نفرین و آفرین قربان خدمت به بشر می کنند و بار سنگین خدمت و اصلاح را بدوش می کشند ، اهداء می کنم This site is dedicated to all Doctors and students that aver the great responsibility of People’s well-being upon their shoulders and carry on their onerous task with utmost dedication and Devotionاولین سایت و ژورنال انتــرنتی علـــمی ،تخـصصی ، پــژوهشــی و آمــوزشــی طبـــی در افغــانســـتان
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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