After reviewing many recordings of major trauma resuscitations, I have come to the conclusion that we are not training our learners on how to perform as a Trauma Team Leader (TTL). They are forced to extrapolate from ATLS, a course never designed for a team at a Level I trauma center. Trauma resuscitations as opposed to medical are a bounded reality. Both the time in the bay and the menu of options are limited--the complete list could be delineated and therefore available for novice TTLs. For a few weeks, I set out to do exactly that. I then sent it out to Chris Hicks (@humanfact0rz) for peer review. His feedback was so good, that I asked him to co-author this project with me. If the response to this project is positive, we will work on the penetrating edition as well.

Blue=cognitive tasks for the TTL

Red=TTL must assign to a subteam (operational)

Solid=always happens in every trauma

Dotted=May happen based on patient injuries or severity

 

* Zero Point Survey

* Team Leadership with Cliff Reid

* EMCrit #230 - Resuscitation Communication

* COMM CHECK: More On Resuscitation Communication

 

 

 

 

* Rapid Infusion Catheter

 

Revised Assessment of Bleeding and Transfusion (RABT)

* Penetrating Trauma

* Shock Index > 1.0

* Pelvic Fracture

* Positive Abdominal FAST

>=2 had sensitivity of 84% and a specificity of 77%

World J Surg 2018;42:3560

5 Sites of Bleeding

* Chest

* Intra-Peritoneal

* Retro-Peritoneal/Pelvis

* Thigh

* Street

 

* Hemostatic Resuscitation by Richard Dutton, MD

* EMCrit Podcast 30 Hemorrhagic Shock Resuscitation

 

 

 

[featimage]

Today on the podcast, I interview Martin Tobin on 3 papers he has recently written on COVID pulmonary physiology.

Martin Tobin

* Praise for Dr. Tobin

* Bio Page

 

Caution about Early Intubation in COVID-19

p-SILI

From 2 studies, 1 on sheep breathing with a human-equivalent Vt of 502 ml

2nd study was observational with a questionable connection to Vt--it was confounded by a number of other factors

Absence of Obtundation

 

L vs. H Subtypes

 

Physio Diversion - Looking for the Patient that needs more Inspiratory Flow

* Tobin Vent Review in NEJM

 

Basing Respiratory Management of COVID-19 on Physiological Principles

Tachypnea in Isolation is Not an Indication for Intubation

Not indicative of increased WOB

Avoiding Intubation with NIPPV

Correlation of saturation with a host of other evils, but it is possible that the saturation is merely a marker--similar to pH. Vicious cycle of shunt, low SvO2, encephalopathy, decreased resp. drive. COVID has been different, with decreased saturation without the horrible lung injury that normally accompanies it. We are also used to patient discomfort from the disease causing the hypoxemia. Retained good compliance. We have not seen the isolated hypoxemia of COVID in many situations before.

 

The Baffling Case of Silent Hypoxemia

Happy Hypoxemia vs. Silent Hypoxemia

Dr. Tobin defines silent hypoxemia as PaO2 < 60 mmHg with a PaCO2 >39 mmHg (as a PaCO2 < =39) blunts the dyspneic response to hypoxemia

Why don't they have dyspnea vs. why do they have such severe hypoxemia unaccompanied by the degree of standard badness that normally accompanies it

They do not crump

They don't develop multi-organ

Dyspnea

Purely subjective

Advanced age and diabetes may blunt dypsnea

Increase in 10 of PaCO2 causes extreme air hunger

Increase Ve when PaO2 <60, but severe hypoxemia elicits increase in ventilation only when PaCO2 > 39 mmHg [32539537]

Definition of Hypoxemia

Do we need to factor in FiO2? Dr. Tobin and I say no!

I define by pulse ox or (PaO2), doesn't matter how much O2. e.g. "He is still hypoxemic despite being placed on NRB."

When does Hypoxemia Become Dangerous?

 

Pulse Ox Inaccuracy

 

OxyHemoglobin Dissociation Curve Shifts

Fever shifts to the right, Decreased CO2 shifts left

Mechanism of Silent Hypoxemia

ACE2 is expressed in the carotid body and may be partially to blame

COVID breaks our Heuristics

Heuristic representation of how bad their lung disease actually is. Projecting expected course...

COVID first disease that unlinks it

Now on to the Podcast...

[featimage]

Today, I am joined by Kei Ouchi to disucss rapid code status discussions in Emergency Medicine and Critical Care. I came across Kei after he put up an amazing post on ALIEM with his co-author Naomi George. Conversation is the essence of palliative care--we need to be experts at them.

Kei Ouchi, MD

Kei Ouchi is an assistant professor of emergency medicine at the Brigham and Women's Hospital in Boston. He splits his time between EM and palliative care research. [@KeiO97]

Kei's and Naomi George's Guide to Rapid Code Status Conversations

More to Read

* ALIEM Post

* Prognosis after intubation study by Kei

* Long-term prognosis after MV (Kei's new study)

* Functional trajectories of older adults after critical illness

* Worse than dying

* How patients experience LTACH

* Median survival is 8 months if older adults are transferred to LTACH

 

How Kei Trained in Palliative Care Conversations

Scott, I realized I’ve never told you anything about how I trained in palliative care communications skills. I keep a record of difficult communication cases from my practice, and I regularly hire actors/role play the encounters with Susan Block (mentor) to get coaching since 2014. She is a master communicator and has been teaching this internationally for the last 35 years. I also completed the following courses and now teach Vital Talk to our trainees with palliative care folks.

* Vital Talk

* Harvard Pall Care Course

Vital Talk is adapted to EM by Corita Grudzen, who is now running a large, national study to see if this makes a difference in patient outcomes.

My ED code status conversation guide is an adaptation of the original Serious Illness Conversation Guide created by Susan Block:

 

 

Kei's Newest Article

* Kei New Article

Now on to the Podcast:

A brief summary of this episode

[featimage]

Today on the podcast, we discuss Neuro-Emergencies and NeuroCritical Care with Neha Dangayach. This is a wide-ranging conversation that you will truly enjoy.

Neha Dangayach

Neha is joining the EMCrit team!!!!!!

Neha S. Dangayach MD, MSCR is an Assistant Professor of Neurology and Neurosurgery. Dr. Dangayach serves as the Director of Neuroemergencies Management and Transfers (NEMAT) for the Mount Sinai Health System, Neurocritical Care Fellowship Director and Research Co-Director for the Institute for Critical Care Medicine (ICCM). She is also a Co-Director of the Mount Sinai Hospital’s busy NSICU and collaborates with a compassionate team to provide world-class patient-centered Neurocritical Care. She leads the Mount Sinai Critical Care Resilience Program (MSCCRP), a multidisciplinary program including intensivists, nursing, social workers, physical, occupation and speech therapists, chaplains, nutritionists among others. Several projects under this program seek to help patients and families cope with ICU recovery. Her research focuses on resilience, spirituality and recovery in critical care; inter-hospital transfers for neuroemergencies and social media in medicine.

Topics of Discussion with Time Stamps

Neha's Slides

* Neurocrit Care Stony Brook Grand Rounds

Neuro-Emergency Management and Transfer (NEMAT) Service

 

Tele-Stroke

Video the CT with phone

2 person job

scroll through every image of axial head ct q 2 seconds

Scroll through CTA MIPs, axial and coronal (sag is a bonus)

 

ICH

Blood Pressure

Specify how often to cycle BP cuff

Ischemic Stroke

 

Who to Intubate and Neuroprotective Intubation

* LAMW: The Neurocritical Care Intubation

 

Which Osmotic Agent for ICP

* Recently Published Guidelines

Platelet Reversal

Recent paper shows no benefit from PLTs or dDAVP in non-neurosurg bleeds [10.1097/CCM.0000000000004348]

Status Epilepticus

Choice of 2nd Line Agent

Keppra 60mg/kg (1/2 the dose in ESRD)

General Anesthetic of Choice is Midazolam

0.2 mg/kg bolus

start infusion 0.2 mg/kg/hr

titrate up every 5 minutes

max 2.9 mg/kg/hr

when getting close to 1mg/kg/hr, give ketamine 1mg/kg followed by 1 mg/kg/hr

Cirrhotics, get propofol

Now on to the Podcast...

Team leadership is hard [duh]. Teaching it to our trainees is even tougher. When you work in a team of true experts with established implicit communication, things just flow--giving the the team leader the impression that they actually know what the hell they are doing. The mark of a good team leader is how they handle a less than ideal team. I found a true master to interview on the topic of team leadership--friend of the show, Cliff Reid.

Attitudinal Choices

* Authoritative vs. empowering

* Be Aware that many of us are helped or hurt by implicit biases

Gender bias paper

* Ju et al. Effect of Professional Background and Gender on Residents’ Perceptions of Leadership. Academic Medicine. 2019 Nov;94:S42–7.

Prep and Prebrief

* Relational Coordination by Purdy et al.

from Purdy et al.

Where to Stand

* Foot of the bed in the opinion of Cliff and me

Zero Point Survey (ZPS)

* Cliff's Video on ZPS

* Perform STEP at the beginning then UP for team recaps

Recap / SitRep / Updates-Priorities

* What am I missing here?

How to Lead from the Follower Slot

* Presupposition

* Pacing and Leading

* Play to their ego

[easyazon_image align="none" height="160" identifier="006124189X" locale="US" src="https://m.media-amazon.com/images/I/51gysFA30GL._SL160_.jpg" tag="emcrit-20" width="105"]

Drive by Voice / Fly by Voice

* Commentary Driving

Eyes On / Eyes Off

Sydney HEMS Team Communication Videos

More from Cliff on EMCrit

* How to Be a Hero with Cliff Reid

* Making Things Happen with Cliff Reid

* Mind of the Resuscitationist with Cliff Reid

* Cliff Reid's Own the Resus Room

Additional Reading

* Resus Communication

* Hicks Human Factors for Teams Summary from Simulcast

* Hicks Fog of War

* Another of those duh studies, but it had to be done -- No difference between EM and surgery resident team leading for trauma

* ABCs of Team Leadership from Regions

* Brindley on followership

Post Publication Peer Review from Iain Beardsell

Chaps,

I really enjoyed the podcast, and having learnt first hand from Cliff I hope I practic...

Today on the podcast, my guest lays out a theoretical framework for the pathophysiology of the lung effects of COVID-19.

Farid Jalali

Dr. Farid Jalali received his Medical Degree from West Virginia University School of Medicine in 2012. He completed his postgraduate training in Gastroenterology at the University of California, Irvine Medical Center in 2018. Dr. Jalali has had extensive training and experience in diagnosing and treating a broad spectrum of GI and Liver disorders. He has a special focus on cancer prevention and spends a great deal of time educating and helping patients on how to prevent cancers in the GI tract and Liver. [@farid__jalali]

Pathophysiology

Potential Treatments

 

Slides from the Presentation

* Farid Jalali COVID-19 Pathophys

Take Home Points from the Talk

* Early endothelial stabilization, before hypoxia sets in, is key to prevent SARS-CoV-2 induced, excess Angiotensin II mediated, intense alveolar capillary vasoconstriction as well as the concomitant pro-inflammatory, pro-thrombotic endothelial milieu, all of which form the basis of lung

injury in COVID19.

* Once hypoxia sets in, supportive care should include early and aggressive endothelial stabilization interventions, properly dosed anticoagulation to prevent lung microvascular thrombi, HFNC, and awake prone position to redistribute flow away from the forming dorsal-predominant intrapulmonary shunts.

* Alveolar capillary microvascular thrombi are not a pre-requisite for the severe lung injury in COVID19, but are a clear step in the wrong direction if allowed to be formed.

* Lung's natural and physiologic protective response to SARS-CoV-2 induced alveolar capillary vasoconstriction and dead-space ventilation is characterized by alveolar hypocapnic bronchoconstriction at the level of the alveolar ducts to reduce a harmful alveolar expansion in these affected capillaries.

* Naturally, unaffected capillaries and corresponding alveoli will have a higher redistribution of ventilation, will exchange more CO2 into alveolar space, and will therefore have hypercapnic bronchodilation.

* This redistribution keeps the lung compliance preserved in the initial lung injury characterized mainly by dead-space ventilation, forming intrapulmonary shunts, without significant interstitial or alveolar edema.

* Compensatory lower inspiratory volumes characterize the patient's response, associated with higher respiratory rate, and "shallow rapid breaths" without distress. [this has not been my experience--EMCrit]

* This lower inspiratory volume is needed to prevent expansion of alveoli in the affected vasculopathic areas, as inappropriate expansion compounds the vasoconstriction in these affected alveolar capillaries.

* This will result in a compensatory tendency to develop hypocapnea on blood gas analysis, often concomitant with hypoxia as intrapulmonary shunts also begin to form as lung injury progress.

* Higher lung volumes, and positive pressure ventilation, disturb the fine balance maintained physiologically in the ventilatory redistribution pattern of the COVID1 9 lung, between high V/Q mismatch areas (poor perfusion, compensatory reduced ventilation to protect against the vasculopathy) and the compensating lower V /Q areas that safely receive higher ventilation in return.

* Therefore, mechanical ventilation may result in worsening of dead-space ventilation by constricting alveolar cap...

This episode continues on from last time's talk by Sara Crager on Right Ventricular Failure. This is a Q&A session with a focus on inhaled pulmonary vasodilators.

Nitric Oxide

Sara likes it through ETT or Hi-Flo NC (can also be done through BIPAP)

Start at 20 ppm

See results within 5-10 minutes

Monitor with CVP

Problems

* Nitric Dioxide (NO2) may be formed which can lead to pulmonary edema or even alveolar hemorrhage.

* MetHb can be formed and some people do routine monitoring for this dyshemoglobinemia.

Additional Resources

* PulmCrit- Inhaled NO for submassive PE: iNOPE or iYEP?

* Review Article on Inhaled NO

 

Epoprostenol (Flolan)

May be more complicated to set-up

go back to marker 5

Epoprostenol @ 0.05 mcg/kg/min

Must have filters on the circuit

* Review Article on Inhaled EpoProst

 

Milrinone

Get the vial, you want 1 mg/ml with 15 mls in vial

5 ml (5 mg) q 6 hours (According to Dr. Crager--may be more frequent if symptoms rebound (down to q 3 hrs))

Ideally use ultrasonic nebulizer

onset ~15 minutes

Must have filters on circuit

LVOTO & RVOTO contraindication for the milrinone

 

respigard!!!

aeroneb pro

must have filters on vent

from Andre Denault Lecture

Additional Resources

* Inhaled Pulmonary Vasodilator Therapy for Management of Right Ventricular Dysfunction after Left Ventricular Assist Device Placement and Cardiac Transplantation

* A multicentre randomized-controlled trial of inhaled milrinone in high-risk cardiac surgical patients

 

Intratracheal Milrinone Bolus for a Crashing Patient

50-80 mcg/kg or 5 mg (1/2 a bolus is also used by some)

onset 4-5 minutes

from the amazing Hospitalist & the Resuscitationist Lecture 2019 by Andre Denault

 

Nitro

Need conc. of 1 mg/ml (standard bottle is 200 mcg/ml)

Doses in studies range from 2.5-25 mcg/kg/min for 10 minutes or 50 ug/kg total given over 8 minutes (perhaps easiest to put 4-5 mg in neb and let it run)

* PulmCrit- Nebulized nitroglycerin: The stealth pulmonary vasodilator hiding under your nose?

Photo by Valeriia Bugaiova on Unsplash

Now on to the Podcast...

We did an amazing episode on EMCrit with Susan Wilcox on Right Heart Failure. However, this oft neglected ventricle deserves even more coverage giving how pesky it can be when it fails. So we brought Sara Crager, MD to Stony Brook to give Grand Rounds. You are going to love this lecture. Part 2 is a Q&A and will be released as a separate episode.

 

This is an embedded Microsoft Office presentation, powered by Office.

 

Now on to the Podcast...

Participants

Josh Farkas

Rory Spiegel

Cameron Kyle-Sidell

Scott Weingart

COVID Low Low PEEP Scale

not for clinical use, just a thought provoker

Personalized PEEP

* [Crit Care 2019;23:412] and

* [Respiratory Care 2020;65(5):583] and

* [Intens Care Med Experimental 2017;5:8]

* Personalize PEEP to Minimize VILI

Now on to the Wee...