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Ultrasound signs of pericardial tamponade with my buddy, Jacob Avila. This episode is simulacasted with Core Ultrasound.

Right Atrial Collapse

greater than 1/3 of the cycle is probably the most specific

 

Right Ventricular Collapse

If the RV is collapsing when the mitral valve is open, then that is specific for tamponade

 

IVC

Lead pipe is specific, flat doesn't rule it out (if pt is volume depleted, etc.)

 

Check Out my Prior Episode with Jacob

* EMCrit 256 - RUSH Redux with Jacob Avila

Steve Alerhand has written a great review article in AJEM

Alerhand-Is it Tamponade?

 

Now on to the Wee...

A brief summary of this episode

I frequently see both residents and attendings inappropriately using ketamine for agitated patients. Inappropriately both by giving it when it is unecessary and giving it in poor fashion when it is indicated.

Our guest today is Reub Strayer

(@emupdates). He is the author of EMUpdates.com. His research and clinical interests include checklists and standardization, airway, legislative work on the treatment of opioid dependence, and an approach to opioid misuse in the ED.

 

Reub breaks agitated patients down in to 3 groups:

1. Agitated, but Cooperative

Not a problem in the ED. Oral medications or non-pharm techniques.

2. Disruptive without Danger

Use standard anti-psychotics and sedatives, with the understanding that Haldol 5mg and Lorazepam 2 mg given IM will take a long time for full effect and even then, may not provide adequate sedation. There are better choices for this group:

* Droperidol monotherapy 5-10 mg IM or 5 mg IV

* Droperidol 5 mg + Midazolam 2mg IM or IV in the same syringe

* Olanzapine 10 mg IM (Needs Resp Monitoring)

* Olanzapine 5 mg + Midazolam 2 mg IM or IV  (Needs Resp Monitoring)

* Haldol 5 mg + Midazolam 2 mg IM or IV (will be slower than the other choices)

If using standard 5/2 (haldol and lorazepam IM), too much time for effect and impatience leads to the wrong subsequent choice, i.e. giving ketamine to this group.

3. Disruptive and Dangerous

* dangerous to staff, dangerous to self

* danger is relative to the resources of the location

Danger could be due to

* The agitation itself or

* An underlying condition that the agitation is preventing from being treated (and may be the cause of the agitation, e.g. tension pneumothorax)

Dividing Line Question: Would you consider intubation to control the situation if ketamine was not available? Reub calls this the Ketamine Litmus Test.

Ketamine takedown must be treated as Procedural Sedation (1:1 nursing observation)

Intramuscular Medication Administration

* Can go through clothes if you need to [Fleming et al.]

* Reub states maximum volume of up to 20 mls per injection

* Harrington 2005 Administer Single Site 30mL Injection Fosphenytoin - Medsurg Nursing

* Hopkins 2013 Large Volume IM Injections Review of Best Practices (Oncology) - Onc Nurse Advisor

* Ramsay 1997 IM Fosphenytoin Loading High Volumes - Epilepsy Research

Ketamine Brain Continuum

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...