MEDEST

For who has a multiyear experience in prehospital emergency medicine and deals everyday with emergency transportation of critical patients the sensation is that the use of emergency warning systems are, mostly of times, useless and doesn’t really have any impact on clinical outcomes. 

But beyond any subjective thought, do we have any evidence on that?

My analysis starts from this article published in 2018 on Annals of Emergency Medicine

by Brooke L. Watanabe, MD et al. and entitled  “Is Use of Warning Lights and Sirens Associated With Increased Risk of Ambulance Crashes? A Contemporary Analysis Using National EMS Information System (NEMSIS) Data”. The authors conclusion says that “Ambulance use of lights and sirens is associated with increased risk of ambulance crashes. The association is greatest during the transport phase. EMS providers should weigh these risks against any potential time savings associated with lights and sirens use.“

Curbside to Beside blog published an interesting post about this topic and resumed the data in this incredibly intuitive infographic

Data extrapolated from
Wantabe et al. (2018)

While ambulances crash rate when using L&S (light and sirens) in the response phase is slightly increased  (7.0 vs 5.4) in the transportation phase the amount of crashes associated with L&S use is significatively higher (17.1 vs 7.0). 

So L&S transportation increases the odd of crash (and this is intuitive) but, on the other side, is there any evidence that use of L&S increases response time and improve clinical outcome?

Fast is Time????

Fabrice Dami et al in an article entitled “Use of lights and siren: is there room for improvement?” found that the time saved with L&S transport was 1.75 min (105 s; P<0.001) in day time and 0.17 min (10.2 s; P=0.27) night-time.

So evidently fast is time, but is a gain of less than 2 min a clinical significative time?

Time is Life???

In 2010 in the article “Emergency Medical Services Intervals and Survival in Trauma:Assessment of the “Golden Hour” in a North AmericanProspective Cohort” concluded that “there was no association between EMS intervals and mortality among injured patients with physiologic abnormality in the field”.

Anderson et al in a 2014 article “Preventable deaths following emergency medical dispatch – an audit study” demonstrated how just 0,2% of the 94.488 “non L&S” dispatched emergencies died in the first 24 hours from the call.  Of those just 0.02% of total “non L&S” emergencies were considered “potentially preventable if the dispatcher had assessed the call as more urgent and this had led to an ambulance dispatch with a shorter response time and possible rendezvous with a physician-staffed mobile emergency care unit”

So mostly of the emergencies are not time sensitive and the clinical outcome does not differ if the transport time is shorter.

Take home messages for our system and for clinical practice

Maybe we need lights and sirens in response phase, cause slightly increase in accident risk corresponds to  some gain in arriving time on the scene.

Maybe we don’t need lights and sirens in transportation phase  cause a great increase in risk of crash do not correspond to a clinical sensitive time gain.

For sure when using L&S we need to be aware that the risk doesn’t worth the price, and even if we use L&S in the varies phases of emergencies pushing the threshold of                security too forward increases the risks and don’t improve clinical benefits for the transported patients.

Clinicians need to be more concerned about performing the right procedures to stabilise patients on pre-hospital phase more than hurrying  with unstable patients toward an unreal Eldorado and risking their own and patients lives. 

Non traumatic Transitory Lost Of Consciousness (TLOC) is a common cause of medical emergency call. Among TLOC Syncope is the most common cause. So the first challenge for an emergency professional is discerning from Syncope and non syncope situations (seizures, psychogenic, other rare causes).

2018 ESC Guidelines for the diagnosis and management of syncope

Syncope according to 2018 Guidelines definition is a “TLOC due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous complete recovery”. 

Among Syncope the causes can be found in vagal reflex (Reflex syncope), a drop in blood pressure due to a deficiency of compensation in a standing position (Orthostatic syncope) and a cardiac cause of syncope (Cardiac syncope)

2018 ESC Guidelines for the diagnosis and management of syncope

But what is the role and what can and must be done on the prehospital field to understand treat and risk stratify a Syncope?

Anamnesis

Is a fundamental step to understand and risk stratify a syncope episode. It has to be targeted to collect all the important informations and to don’t loose precious time.

We can divide the information we collect in two categories.

The first kind of information we area going to ask (to bystanders and patients) is about the syncope event.

• How much the lost of consciousness lasted
• How it happened (standing, sitting or laying)
• What was the patient doing (resting or during exercise)
• What the patient felt before the syncope (palpitations, chest pain, dyspnea, dizziness, other)
• What happened during or immediately after the syncope (seizures, other)

Second step is collecting informations about the patient medical conditions. We have to focus on

• What medical condition he actually suffers or suffered in the past
• Which kind of drugs he is actually doing

After a focus anamnesis the second step is about the physical exam of the patient.

Diagnostic tests

During physical exam a rapid general neurologic and cardiac examination has to be completed, but two additional steps need to be done in a syncope patients

• Orthostatic challenge in active standin position
• Carotid sinus massage (CSM) in patients aged >40 years.

Orthostatic challenge:  Standing BP evaluation has to be done after 3 minutes of active standing position with the patient fully monitored, and “abnormal BP fall is defined as a progressive and sustained fall in systolic BP from baseline value >_20 mmHg or diastolic BP >_10 mmHg, or a decrease in systolic BP to <90 mmHg” (European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope).

Carotid sinus massage: A ventricular pause lasting >3 s and/or a fall in systolic BP of >50mmHg is known as carotid sinus hypersensitivity. “Carotid sinus syndrome (CSS) There is strong consensus that the diagnosis of CSS requires both the reproduction of spontaneous symptoms during CSM and clinical features of spontaneous syncope compatible with a reflex mechanism.” (European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope)

12 leads EKG

It’s a fundamental diagnostic tool and has to be performed in all syncope patients.

What are the risky features we have to consider when looking to ann EKG of a syncope patients:

At least 6:

1. Ischemia
2. Arrithmia
3. Pre-excitation/WPW
4. Brugada pattern
5. Hypertrophic cardiomyopathy
6. Arrhythmogenic Right Ventricular Cardiomyopathy

POCUS

Is there a role for Point of Care Ultrasound in differential diagnosis and risk stratification of syncope.

Probably yes cause we can look at:

• Aorta for dissection
• VD/VS ratio for PE
• Pericardium for effusion
• EF for cardiac function evaluation

High risk VS non high risk syncope

At the end of those steps the prehospital professional has two chances.

1. There is a likely cause of syncope
2. The syncope is of unknown cause

2018 ESC Guidelines for the diagnosis and management of syncope

If the cause is known or very likely we have to follow the specific pathway.

In the unknown syncope we have to stratify the risk.

In prehospital field is important to look for high risk features of syncope:

• History of heart failure or other cardiac conditions
• Syncvope in supine position
• Syncope during excercise
• Dyspnea before or immediately following syncope
• Palpitations before syncope episode
• EKG abnormalities
• Persisting low blood pressure (SBP<90 mmHg) in supine positi
• Orthostatic Hypotension

Each one of those is indicative of high risk prehospital features and the patient need further ED examination.

In all other cases the clinician can decide case by case if the patient can be treated out of the hospital or need admission to ED.

References :

Michele Brignole, Angel Moya et al. European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope

Third step of 1 YEAR IN REVIEW, the classical end of year MEDEST appointment with all that matter in emergency medicine literature.

In this post we review the 2018 Trauma papers divided by topic.

So let’s start

• Traumatic Brain Injury

Effect of Early Sustained Prophylactic Hypothermia on Neurologic Outcomes Among Patients With Severe Traumatic Brain Injury. The POLAR Randomized Clinical Trial.

Rapid Sequence Intubation in Traumatic Brain-injured Adults

Brain Oxygenation Optimization After Severe Traumatic Brain Injury: An Ode to Preventing Brain Hypoxia

Management of traumatic brain injury patients

Efficacy of pre-hospital rapid sequence intubation in paediatric traumatic brain injury: A 9-year observational study

Pediatric traumatic brain injury—a review of management strategies

• Traumatic cardiac arrest

Traumatic arrest & the HOTTT Drill

EMERGENCY MEDICAL SERVICES SIMPLE THORACOSTOMY FOR TRAUMATIC CARDIAC ARREST: POSTIMPLEMENTATION EXPERIENCE IN A GROUND-BASED SUBURBAN/RURAL EMERGENCY MEDICAL SERVICES AGENCY

• Hemorrhagic shock

Plasma-first resuscitation to treat haemorrhagic shock during emergency ground transportation in an urban area: a randomised trial.

Prehospital Plasma during Air Medical Transport in Trauma Patients at Risk for Hemorrhagic Shock

What fluids are given during air ambulance treatment of patients with trauma in the UK, and what might this mean for the future? Results from the RESCUER observational cohort study

Evaluation of tranexamic acid in trauma patients: A retrospective quantitative analysis

Efficacy of prehospital administration of tranexamic acid in trauma patients: A meta analysis of the randomized controlled trials

Prehospital haemostatic dressings for trauma: a systematic review

Resuscitative endovascular balloon occlusion of the aorta performed by emergency physicians for traumatic hemorrhagic shock: a case series from Japanese emergency rooms

Resuscitative Endovascular Balloon Occlusion of the Aorta and Resuscitative Thoracotomy in Select Patients with Hemorrhagic Shock: Early Results from the American Association for the Surgery of Trauma Aortic Occlusion in Resuscitation for Trauma and Acute Care Surgery Registry

Permissive Hypotension vs. Conventional Resuscitation Strategies in Adult Trauma Patients with Hemorrhagic Shock: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Trauma ‘Code Crimson’ Pathway. Streamlining access to definitive intervention for patients with life-threatening haemorrhage

• Pediatric

Pediatric airway management devices: an update on recent advances and future directions

Cricoid Pressure During Induction for Tracheal Intubation in Critically Ill Children: A Report From National Emergency Airway Registry for Children

• The rest

Pre-hospital emergency anaesthesia in awake hypotensive trauma patients: beneficial or detrimental?

Circulation first – the time has come to question the sequencing of care in the ABCs of trauma; an American Association for the Surgery of Trauma multicenter trial

Damage Control for Vascular Trauma from the Prehospital to the Operating Room Setting

Ultrasonography Assessments of Optic Nerve Sheath Diameter as a Noninvasive and Dynamic Method of Detecting Changes in Intracranial Pressure

Issues and challenges for research in major trauma

Effect of hypoxia on mortality and disability in traumatic brain injury according to shock status: A cross-sectional analysis

Second step of 1 YEAR IN REVIEW, the classical end of year MEDEST appointment with all that matter in emergency medicine literature.

In this post we review the 2018 Airway management literature of note divided by topic.

So let’s start

• Bag mask ventilation

Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest. A Randomized Clinical Trial

• Extraglottic Devices

Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest. A Randomized Clinical Trial.

Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of Hospital Cardiac Arrest on Functional Outcome. The AIRWAYS-2 Randomized Clinical Trial.

Preliminary Report: Comparing Aspiration Rates between Prehospital Patients Managed with Extraglottic Airway Devices and Endotracheal Intubation.

Pre-hospital i-gel blind intubation for trauma: a simulation study.

Supraglottic airway devices: indications, contraindications and management.

Laryngeal mask airway versus bag-mask ventilation or endotracheal intubation for neonatal resuscitation.

Self-pressurized air-Q intubating laryngeal airway versus the LMA ClassicTM: a randomized clinical trial.

• Intubation, Direct Laryngoscopy, Airway management

Endotracheal Intubation for Traumatic Cardiac Arrest by an Australian Air Medical Service.

Effect of Cricoid Pressure Compared With a Sham Procedure in the Rapid Sequence Induction of Anesthesia. The IRIS Randomized Clinical Trial.

Effect of Use of a Bougie vs Endotracheal Tube and Stylet on First-Attempt Intubation Success Among Patients With Difficult Airways Undergoing Emergency Intubation. A Randomized Clinical Trial.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Tracheal intubation in critically ill patients: a comprehensive systematic review of randomized trials.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Airway Management During Out-of-Hospital Cardiac Arrest

Assessing Advanced Airway Management Performance in a National Cohort of Emergency Medical Services Agencies

• Video Laringoscopy, VL vs DL

Comparison of video laryngoscopy versus direct laryngoscopy for intubation in emergency department patients with cardiac arrest: A multicentre study.

First attempt success with a Macintosh-style video laryngoscope is high whether or not the video screen is viewed.

Should the Glidescope video laryngoscope be used first line for all oral intubations or only in those with a difficult airway? A review of current literature.

Comparison of King Vision video laryngoscope and Macintosh laryngoscope: a prospective randomized controlled clinical trial.

Interpreting the Cormack and Lehane classification during videolaryngoscopy.

Intubation with cervical spine immobilisation: a comparison between the KingVision videolaryngoscope and the Macintosh laryngoscope. A randomised controlled trial.

Videolaryngoscopy versus direct laryngoscopy for emergency orotracheal intubation outside the operating room: a systematic review and metaanalysis

• Guidelines, clinical policies and more

Guidelines for the management of tracheal intubation in critically ill adults.

Airway Management for Trauma Patients

Pragmatic Airway Management in Out-of-Hospital Cardiac Arrest

Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia

The Vortex model: A different approach to the difficult airway

Airway management in critical illness: practice implications of new Difficult Airway Society guidelines

Airway Management Practice in Adults With an Unstable Cervical Spine: The Harborview Medical Center Experience

Defining the criteria for intubation of the patient with thermal burns

Shifting Priorities from Intubation to Circulation First in Hypotensive Trauma Patients

Airway and ventilation management strategies for haemorrhagic shock. To tube, or not to tube, that is the question!

Advanced airway management in hoist and longline operations in mountain HEMS. Considerations in austere environments: a narrative review This review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM)

• Pediatric

Pediatric airway management devices: an update on recent advances and future directions

Cricoid Pressure During Induction for Tracheal Intubation in Critically Ill Children: A Report From National Emergency Airway Registry for Children

• Drugs

Emergency Department Intubation Success With Succinylcholine Versus Rocuronium: A National Emergency Airway Registry Study

Rapid Sequence Intubation in Traumatic Brain-injured Adults

• The rest

How much experience do rescuers require to achieve successful tracheal intubation during cardiopulmonary resuscitation?

Clinical Myth #1. All heart failure/cardiogenic pulmonary edema (HF/CPE) patients are fluid overladed .

Scientific Truth #1: Just a small part of heart failure/ cariogenic pulmonary edema (HF/CPE) patients are fluid overloaded. Most (>50%) patients are redistributed (from splanchnic circulation and lover limb to pulmonary circle). Use your clinical judgement (poor sensitivity and specificity) or ultrasound (lung US for the presence of ≥3 B lines in ≥2 bilateral thoracic lung zones is reliable and sensitive for pulmonary edema) to establish which kind of patient you are dealing with: Overloaded or Redistributed. That makes the difference.

Clinical Myth #2. All HF/CP patients benefit from diuretic ( Furosemide or other diuretics) therapy.

Scientific Truth #2: Just normotensive overloaded HF/CPE patients can benefit from diuretic ( Furosemide or other diuretics) therapy.

Furosemide can be detrimental on short and long term outcome because:

• decreases LV function, increasing ventricular filling pressure 

• increases systemic vascular resistance through activation of the renin-angiothensyn system

• decreases glomerular filtration rate

Clinical Myth #3. Nitrates small doses continuous infusion is the right strategy in HF/CP patients.

Scientific Truth #3: Nitrates and Non Invasive Positive Pressure Ventilation are effective first line interventions in hypertensive HF/CPE patients.

High doses Nitrates administration is safe. 2 mg bolus of nitrates every 3 min in hypertensive patients (with close blood pressure check) are safe and faster in achieving clinical targets and symptoms relief. 

Clinical Myth #4. Morphine is safe and effective in HF/CP patients because relief anxiety and reduce preload, and has to be part of first line interventions.

Scientific Truth #4: Morphine administration has no evidences of clinical benefit in HF/CPE patients and is not part of first line treatment for HF/CPE patients. Low quality evidence suggests that morphine is associated with worse outcomes when compared to patients not receiving opioids.

Clinical Myth #5. In hypotensive (cariogenic shock) HF/CP patients Dopamine is the first choice vasopressor.

Scientific Truth #5: Norepinephrine is the first line medication to reach target mean arterial pressure and achieve organ perfusion, rather than Dopamine. Evidence suggests that norepinephrine is associated with improved outcomes including
lower mortality and lower risk of dysrhythmia when compared with Dopamine.

Bottom Line Clinical Pearl: Use ultrasound during every step of your clinical pathway in HF/CPE patients.

• US detection of B-lines for diagnosis in undifferentiated dyspneic patients

• US of IVC to discriminate between fluid overloaded or redistributed patients

• Pump/Tank/Pipes US approach for differential diagnosis in undifferentiated shock patients

Liberally adapted from:

Brit Long MD, Alex Koyfman, MD,  Eric J. Chin, MD. Misconceptions in acute heart failure diagnosis and Management in theEmergency Department. American Journal of Emergency Medicine. 2018 Sep;36(9):1666-1673. doi: 10.1016/j.ajem.2018.05.077. Epub 2018 Jun 1

References:

Myth #1

• Fallick C, Sobotka PA, Dunlap ME. Sympathetically mediated changes in capacitance: redistribution of the venous reservoir as a cause of decompensation. Circ Heart Fail 2011;4:669–75.
• Zile MR, Bennett TD, St John Sutton M, et al. Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures. Circulation 2008 Sep 30;118 (14):1433–41.
• Chaudhry SI,Wang Y, Concato J, Gill TM, Krumholz HM. Patterns of weight change preceding hospitalization for heart failure. Circulation 2007;116:1549–54
• Viau DM, Sala-Mercado JA, Spranger MD, et al. The pathophysiology of hypertensive acute heart failure. Heart 2015;101:1861–7.
• Jambrik Z, Monti S, Coppola V, et al. Usefulness of ultrasound lung comets as a non radiologic sign of extravascular lung water. Am J Cardiol 2004;93(10):1265–70.
• Mallamaci F, Benedetto FA, Tripepi R, et al. Detection of pulmonary congestion by chest ultrasound in dialysis patients. JACC Cardiovasc Imaging 2010;3(6):586–94.
• Anderson KL, Fields JM, Panebianco NL, et al. Inter-rater reliability of quantifying pleural B-lines using multiple counting methods. J Ultrasound Med 2013;32(1):115-20.

Myth #2

• Francis GS, Siegel RM, Goldsmith SR, et al. Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Ann Intern Med 1985;103(1):1–6.
• Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124–8.

Myth #3

• Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351:389–93.
• Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.
• Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate i safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.

Myth #4

• Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema. Emerg Med Australas 2008;20:384–90.
• Vasko JS, Henney RP, Oldham HN. Mechanisms of action of morphine in the treatment of experimental pulmonary edema. Am J Cardiol 1966;18:876–83.
• Kaye AD, Hoover JM, Kaye AJ, et al. Morphine, opioids, and the feline pulmonary vascular bed. Acta Anaesthesiol Scand 2008;52:931–7.
• Riggs TR, Yano Y, Vargish T. Morphine depression of myocardial function. Circ Shock 1986;19:31–8.
• Miró Ò, Gil V,Martín-Sánchez  FJ, et al.Morphine use in the ED and outcomes of patients with acute heart failure: a propensity score-matching analysis based on the EAHFE registry. Chest 2017 Oct;152(4):821–32.

Myth #5

• Rui Q, Jiang Y, Chen M, et al. Dopamine versus norepinephrine in the treatment of cardiogenic shock: a PRISMA-compliant meta-analysis. Medicine 2017;96(43):e8402.

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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?

1. Looking for reversible causes
2. Monitoring perfusion
3. 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:

1. ALWAYS use ultrasound to determine cardiac activity in cardiac arrest patients
2. Don’t trust central pulse palpation
3. Pseudo PEA is an ultrasound evident cardiac activity without carotid pulse
4. Pseudo PEA is a big clinical reality beyond ACLS mantras
5. Use ultrasound to look for reversible causes of pseudo PEA.
6. Use waveform EtCO2 and waveform Pulse Oximetry to monitor perfusion
7. 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
8. 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