Shadowboxing

First brought to my attention by Gary Klein in EMCrit 179, shadowboxing is considered one of the best ways to relay tacit knowledge. Shadowboxing has a situation presented to an expert with a pause before they answer at critical junctions. During the pause, the learner should mentally commit to what they are thinking and what they would do.

Today's Participants

One of our regulars is one of my former fellows, Ryan (Barney) Barnicle.

Ryan Barnicle

Ryan Barnicle is one of the newest faculty in the Education Section at Yale University School of Medicine’s Department of Emergency Medicine. He completed his emergency medicine residency at Stony Brook University Hospital followed by fellowship in Advanced Resuscitation. A former high school teacher, he has maintained his passion for teaching with residents and medical students. His interests include resuscitation education and critical care echocardiography.

Christina Lu

Christina Lu completed her fellowship in Advanced Resuscitation and emergency medicine residency at Stony Brook University Hospital. She is an Assistant Professor of Emergency Medicine and currently serves as the Associate Director of the Emergency Critical Care and Resuscitation Fellowship, and Associate Director of the Emergency Critical Care Division at Hartford Hospital. She has an interest in critical care education and advancing the field of resuscitation medicine.

Guest Presenting Resident: Samy Chettat

Originally from Denver, CO (GO BRONCOS). Undergrad CU Boulder (GO BUFFS), Medical School Drexel (Go DRAGONS). Big sports fan. Completed residency at, and now a Toxicology Fellow at OHSU. Special interest in animal/plant poisonings and Critical Care Toxicology.

The Case

Here is the case, in the order of which information was available real time.

EMS called a CODE 3 – ETA of 5 minutes with only limited information: “39-year-old patient has a history of ‘tracheomyeloma’ whose CPAP machine broke and was found down, cyanotic, currently being bagged.”

Q: How does airway management priorities change when a patient is being manually ventilated by EMS? How/when do you transition to ED staff? What do you look for to ensure BVM is being done appropriately?

A: BVM ventilation should be done with two people, one sealing + one bagging. Ideal face-to-mask sealing is done with two hands. BVM should include PEEP valve, ETCO2 monitor (tested prior to patient arrival if possible), and flush rate supplemental oxygen. If needed, a SGA such as an i-Gel can be used to also preoxygenate with PEEP but operator must hold the SGA with constant downward/inward force to maintain seal around glottic structures.

For more information on the Ultimate BVM, see the prior EMCrit episode here: https://emcrit.org/emcrit/ultimate-bvm/

So she rolls in getting manually ventilated, but was reportedly “easy” to ventilate, and was oxygenating with SpO₂ >95%.

Frame of reference, this is a community sites with really no nursing staff that is comfortable or experienced with critical care.

Initial vitals HR 95, T 97.6F, RR 5 (though being bagged every ~5 sec). Initial BP took a while to get due to patient’s arm size and equipment malfunction. BGL was ok, ~150s
General Appearance: Obtunded
HEENT: No evidence of trauma, Pupils constricted, reactive, not pin-point
Cardio: RRR, no murmurs, not cyanotic, not mottled, not cold extremities. Obese but no pitting edema
Pulm: Bilateral coarse lung sounds, no stridor
Abd: soft, non-distended
Neuro: withdraws extremities to painful stimuli

Since she was easily bagged, decided there was time to optimize before intubation. Established bilateral large bore IVs. Got BP which was initially 138/64.

Q: EMCrit listeners know how to optimize before intubation in general but what are the unique features of this case that should be considered?

A: Consider a large empiric dose of Narcan of opioid overdose is in the ddx but not obvious. If it fails, move on. Patients should not be preoxygenated while laying flat and obese patients oftren require higher PEEP in order to obtain adequate SpO₂. Preoxygenation devices/strategies include modified BVM, CPAP w/ ventilator, HFNC, and SGA if necessary.

EKG: NSR, narrow complex, no ST segment changes suggesting ischemic event.

Ultrasound was being used elsewhere but sent someone to get it. Got optimized positioning for intubation with multiple backups given “tracheomyeloma” history.

Note: (We had assumed they probably meant “tracheomalacia” but prepared for potential difficult airway just in case there was some sort of head/neck cancer.)

Q: In layman’s terms, tracheomalacia is essentially a collapsing trachea. Can be congenital or acquired. What are some important considerations when it comes to intubating a patient with known or suspected tracheomalacia?

A: Tracheomalacia should not effect intubation itself and EPs should proceed with a technique they are comfortable with, though awake intubation is always an option of anatomical variance is a concern. Preoxygenation may require positive pressure ventilation with PEEP though.

Overview of Tracheomalacia can be found here: https://www.ncbi.nlm.nih.gov/books/NBK553191/

Yang D, Cascella M. Tracheomalacia. 2022 Jul 9. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 31985984.

Once optimized, we prepared for intubation. We did happen to have the luxury of getting patient’s medication list and saw she took morphine for chronic pain. So just prior to intubation, we decided to trial a dose of Narcan.

Q: We are hoping this works and an intubation might be avoided. The patient has respiratory depression and altered mental status with a pupil exam that supports is consistent with opioid toxicity. This seems like a reasonable indication for a trial of Narcan. Would you go for the intubation or see if Narcan works? When should Narcan be avoided? What are some adverse effects that should be anticipated? What dose are you trying for someone so ill?

A: Avoid Narcan in cardiac arrest. It does not help the situation and makes things potentially worse from a pulmonary edema standpoint if ROSC is obtained. Large doses should be used in critically ill patients, deal with withdrawal afterwards.

The latest AHA guidelines do not endorse giving naloxone to patients in cardiac arrest: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000918

Merchant RM, Topjian AA, Panchal AR, Cheng A, Aziz K, Berg KM, Lavonas EJ, Magid DJ; Adult Basic and Advanced Life Support, Pediatric Basic and Advanced Life Support, Neonatal Life Support, Resuscitation Education Science, and Systems of Care Writing Groups. Part 1: Executive Summary: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020 Oct 20;142(16_suppl_2):S337-S357. doi: 10.1161/CIR.0000000000000918. Epub 2020 Oct 21. PMID: 33081530.

Narcan 0.4 mg was pushed. Within 1 min patient woke up, coughing, breathing on her own. After a few minutes of disorientation, was awake and talking. Though couldn’t give us much history. She said in general she was feeling fine and denied chest pain, abdominal pain, nausea, vomiting.

Her mother also arrived at that time and gave additional history, which is where the complexity of this case comes in:

“[Patient] had been having recurrent cough and got a bronchoscopy a couple of months ago and was diagnosed with tracheobronchomalacia, and an echocardiogram at that time revealed she  also had pulmonary hypertension. She was to see a pulmonologist next month for further workup. She was also recently diagnosed with moderate obstructive sleep apnea and was prescribed CPAP at night which she has been using intermittently due to tolerance issues. She was diagnosed with pneumonia last week and has been taking Augmentin.”

At this time, she started to have critical desaturations below SpO₂ 90%

Q: What is the differential diagnosis for this new hypoxemia in this patient? How are we going to investigate or manage this?

A: There is a broad differential but next steps should include CXR, ABG/VBG, POCUS Blue Protocol (or other lung assessment protocol), initiation of NIPPV. As always, preparation for intubation if needed. If available, getting recommendations from the patient’s pulmonologist at this point may be reasonable.

With her history, we did start BPAP. Mental status continued to improve with BPAP. Overall, thought we cracked the case, this was morphine overdose coupled with some CO2 narcosis, problem solved. What were settings of BPAP? 15/8

CXR:  Low lung volumes but no obvious consolidation, bibasilar atelectasis

No point of care labs were available at this hospital, so initial labs eventually get back with these notable values:

VBG: pH 7.15, pCO2: 69, Bicarb: 23, Lactate of 1.4 à primary respiratory acidosis

CBC: WBC 20, no anemia, normal plt à leukocytosis

CMP: Cr 4.21, K 6.3 GFR 10 (previously normal kidney function) à acute kidney injury, hyperkalemia

HsTrop: 800 à NSTEMI

Q: How do we adjust our hyperkalemia treatment for patients in AKI or with CKD?

A: Hypoglycemia is a reasonable concern with AKI/CKD. 10 U of insulin should always be given with two doses of D50 (or the equivalent). Consider reducing to 5 U and repeating as necessary. Calcium will likely not hurt this patient. Avoid sodium bicarbonate.

A great recent review of hyperkalemia treatment and typical controversies can be found here: https://pubmed.ncbi.nlm.nih.gov/34890894/

Gupta AA, Self M, Mueller M, Wardi G, Tainter C. Dispelling myths and misconceptions about the treatment of acute hyperkalemia. Am J Emerg Med. 2022 Feb;52:85-91. doi: 10.1016/j.ajem.2021.11.030. Epub 2021 Nov 27. PMID: 34890894.

Gave albuterol, insulin/d50, calcium gluconate for potassium

About 1 hour into the case, BP started down trending with SBPs in the 80s, but MAP hovering around 60-65, her mental status also hadn’t declined. She was still briskly answering questions appropriately but did seem pretty tired overall.

With that kidney function, foley catheter was placed for close ins and outs and to identify urine production.

Trialed 1L Lactated Ringers did not improve her BP.

POCUS of heart showed plump IVC, a few b-lines, and per my read (admittedly not the greatest sonographer) mildly depressed EF, mildly dilated appearing ventricles. No pericardial effusion.

So continued to be hypotensive now with MAP in the high 50s, she was also getting less responsive.

Why is this patient decompensating? How would you manage the blood pressure?

Our considerations/DDx at this point:

• MI à cardiogenic shock: Bump in trop, but no chest pain, risk factors, or EKG changes
• Septic Shock: Leukocytosis, hx of recent pneumonia. But not febrile, not tachy
• PE: Though she had just been HD stable, and near normal after getting Narcan. So she would have had to suddenly develop a massive PE, which I guess could be possible but this was lower on the list of suspects.
• Underlying Pulmonary HTN exacerbation
• Need for redose of Narcan

The attending and I had a discussion about how best to proceed. With reported history of pulmonary hypertension, which given young age, probably not related to bad heart but to her respiratory pathology. Given POCUS looking like global depressed cardiac function, and appearing generally volume up, we opted to not give additional fluids. Discussed vasopressor choice and decided to start with NE low dose and see what happens and then add vasopressin as a second line with the thought being to try to increase coronary perfusion first and then think about pulmonary dilators next.

Repeat VBG was resulted and showed:

pH: 7.23 PCO2 47, Bicarb: 19 à improved respiratory acidosis, but now with slight metabolic compenent

BP consistently low now on 30mcg/min of NE (weight of patient was 124kg). Though hospital policy cannot exceed 30mcg/min.

Patient was re-dosed with Narcan 0.4mg with no change, and now declining mental status on BPAP.

ICU was finally able to come evaluate the patient and recommended intubation based on the repeat gas, more IVF, and agreed with adding vasopressin with the thinking that the pH being low is making the NE not effective.

Q: What is your differential for failing vasopressors? Do you want to give this patient more fluids? How does pH affect your choice of pressors? What are you doing to address the acidosis?

A: Everyone should have a differential for failing vasopressors (Dr. Swaminathan discusses a list of considerations here: https://emergencymedicinecases.com/em-quick-hits-june-2021/.) In truth, this patient has not failed norepinephrine at these doses and hospital policy should be confirmed before limiting to 30mcg/min as evidence suggests much higher doses are acceptable and safe. If pHTN is truly a consideration, more IVFs should be given very cautiously. In severe RV failure, diuresis is often needed but this patient was not in severe RV failure. pH only affects vasopressors at dramatically low numbers < 7. This patient’s acidosis is NOT affecting NE effectiveness. Consider your differential. Consider adding a true inotrope (epinephrine or milrinone).

A great overview of Pulmonary Hypertension and RV Failure was discussed on EmCrit previously here  with Dr. Wilcox (https://emcrit.org/emcrit/pulmonary-hypertension-right-ventricular-failure/ ) with the primary source being found here: https://pubmed.ncbi.nlm.nih.gov/26342901/

Wilcox SR, Kabrhel C, Channick RN. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Ann Emerg Med. 2015 Dec;66(6):619-28. doi: 10.1016/j.annemergmed.2015.07.525. Epub 2015 Sep 3. PMID: 26342901

For more on the safety of peripheral vasopressors, see this recent systemic review & meta-analysis: https://pubmed.ncbi.nlm.nih.gov/33039229/

Tran QK, Mester G, Bzhilyanskaya V, Afridi LZ, Andhavarapu S, Alam Z, Widjaja A, Andersen B, Matta A, Pourmand A. Complication of vasopressor infusion through peripheral venous catheter: A systematic review and meta-analysis. Am J Emerg Med. 2020 Nov;38(11):2434-2443. doi: 10.1016/j.ajem.2020.09.047. Epub 2020 Sep 28. PMID: 33039229.

Vasopressin started and the patient transported to ICU. Intubation deferred to ICU team.

Hospital Course:

First 24 hours:

The patient was started on vasopressin and her blood pressure improved. The team also started a naloxone infusion, but respiratory effort remained poor and she was intubated successfully by the ICU team.

Q: I think we are now suspecting that pHTN might be contributing at least partially to her hemodynamics and respiratory failure here. How do we modify our intubation technique for someone we suspect has pHTN or RV failure?

A: Avoid intubation when possible but if force to intubate due to mental status changes, consider an awake intubation as part of a hemodynamically neutral transition to the ventilator.

• Initial vent settings in ICU: RR 24, VT 470, FIO2 50%, PEEP 5

• VBG 1 hour post intubation: pH 7.48, pCO2 27, HCO3 20

• Patient extubated the next morning, to BPAP à NC

• Total Vent Time: <12 hours

• CK resulted after she left ED and was ~3000

• Got a total of 4L IVF the first day as part of her treatment of rhabdomyolysis

• Weaned NE within 6 hours and vasopressin within 8 hours

• AM labs showed

CBC: WBC 11.9, Hb 10.3, plt 202

CMP: Na 135, K 3.1, BUN 24, Cr 1.86, GFR 35

CK: 3000à2272

hsTrop: 800à773

• Formal echo interpretation:

∑     Poor quality imaging

∑     Normal left ventricular size and systolic function with LVEF of 65%.

∑     There is pulmonary hypertension. Estimated right ventricular systolic pressure (RVSP) is 45 mmHg.

∑     Mild tricuspid regurgitation.

∑     There are no prior studies for comparison.

NB: RVSP ~ sPAP. 45 = Moderate pHTN

Q: If someone has known severe pHTN or obvious acute RV failure, how should we modify our IVF use?

A: Avoid, when possible. Diuresis may be necessary. This case did not meet this criteria.

Ultimately, patient treated for sepsis with presumed respiratory source given her recent pneumonia. She continued IV antibiotics. Blood cultures never turned positive. She ended up staying for a total of 4 days, complicated by diarrhea ~7x daily that was eventually attributed to her antibiotics. She also took some time to wean off nasal cannula. Lab work continued to improve and by hospital day 4, she was at her baseline kidney function, tolerating PO, ambulatory, and on room air.

She was seen by pulmonology in hospital for her tracheobronchialmalacia. Ultimately, there was no immediate recommendations from pulmonology but planned to see her as an outpatient. They thought her initial presentation was multifactorial but likely triggered by community acquired pneumonia and complicated by decreased CPAP compliance  (because she stopped using the mask because she was having a productive cough) which was complicated by her underlying tracheobronchialmalacia. From pulmonary consult note:  “Inspection bronchoscopy, which showed 90% collapse of the distal trachea and mainstem bronchi even down to the right lower lobe. The segmental airways remained > 50% patent during inspiration and expiration.”

Summary: She was hypotensive and had respiratory failure with acute kidney injury, but hemodynamics improved with fluids and vasopressors, which were weaned within a few hours. Required a short time on vent. Kidney function quickly improved.

Multi-factorial Altered Mental Status: toxic encephalopathy / hypercarbic encephalopathy / uremic encephalopathy

Mixed Respiratory Failure: multifactorial complicated by tracheobronchialmalacia history, obesity-hypoventilation syndrome, CAP, morphine toxicity

Multi-factorial Shock: probably components of cardiogenic, septic, hypovolemic shock

Multi-factorial Acute Kidney Injury: pre-renal (hypovolemia), intrinsic (ischemic ATN, rhabdomyolysis)

Questions/Considerations:

Logistical issues at smaller community hospitals:

-I wanted to place an A-line early on when she was persistently hypotensive, however no nursing staff had the training, and the ED didn’t even stock a-lines apparently.

-I was flabbergasted and thought everyone was joking about the maximum dose of NE being 30mcg/min, but they were dead serious and all nursing staff and attendings seemingly agreed, and as a resident in the moment had me questioning my own reality, so I went with it.

Learning points from the case/retrospective questions:

-Should Narcan be a standard part of my respiratory distress/respiratory code package? I don’t see the harm other than producing massive withdrawal in select patients. Is .4mg a good trial dose? Or in a peri-code situation should we just go big, incase it’s a Narcan resistant substance?

-Any quick things I can do on POCUS to help decide if her condition was related to pulmonary hypertension?

-What critical care considerations do you take in the ED regarding pulmonary hypertension?

-PE is a possibility but everyone was hyper-aware of her kidney function and thought CTA would be more harmful than helpful—In this scenario, contrast induced nephropathy was not a concern of mine. Once BP improved we should have just checked for a PE right?

-Chicken or the Egg? Did she have some sort of insult to kidneys which caused ARF and cause a “renal overdose” of her morphine and then hypoxia related multiorgan failure, or other way aroundà Morphine ODà hypoxic multiorgan injury. Notably, she denied taking any morphine today, had no thoughts of self harm.

-Was our thinking on pressor order correct (NE then vaso)? Should we have just trialed pulmonary dilators or inotropes?

-Was intubation a critical missed step? With that second VBG? In the moment I thought that was generally improved and that Intubation with PPV could potentially cause more harm by decreasing her venous return.

-If someone is on pressors already, will administering sedation medications have any clinically significant effect on BP? Anything more we could do to optimize BP prior to intubation if the patient wasn’t taken to ICU

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Scott Weingart, MD FCCM

Editor-in-Chief, at EMCrit.org

An ED Intensivist from NY.
Professor
Nassau University Medical Center
No conflicts of interest (coi).

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