I heard this in Paramedic School, and I heard this in Nursing School: ”Listen to what your gut is telling you.” I did not pay much attention to it, and I wondered, if I am listening to my gut, why am I paying all this money for you to teach me? But this is what I have learned since then – although my gut sometimes leads me astray, this was NOT one of those instances.
The Case
Our transport team was called to a small critical access hospital three miles from the state line for a 59-year-old male presenting that afternoon with an one-week history of shortness of breath (SOB), recurring fevers, loss of taste / smell and general malaise. His Rapid COVID-19 swab was positive. He did not have a blood gas drawn, but his anion gap was normal, and he had a serum lactate of 3 mmol/L.
Our pre-arrival information included a reported initial pulse oximetry value in the 60% range with a respiratory rate in the 40-50 breaths per minute (bpm) range. As a result of this, he was immediately placed on BiPaP. The chest x-ray findings per the sending physician included diffuse infiltrates bilaterally (minus the ground glass appearance that I was expecting). He was hemodynamically stable following one, 1-liter crystalloid bolus.
With those numbers, our initial plan definitely included intubation. Yet, we were a little puzzled why the referring physician did not have the patient intubated already. Per our current policy, we do not transport COVID-positive patients on BiPaP due to the high risk for aerosol generation in the confined space of an aircraft cabin (rotor- or fixed-wing). With that said, we walked into the patient’s room, fully prepared to take control of the airway.
However, my initial impression changed when I met our patient. He was talking in complete sentences, he was purposeful, and he was very reluctant to go with us. He stated, “I know what is wrong with me, and I would rather convalesce at home” (the fact that convalesce came out of his mouth made me reluctant to transport him at all). With that said, he was still tachycardic, very tachypneic, with an oxygen saturation in the low to mid 80% range.
The fact remained that we could not transport this patient on BiPap, so our plan was to trial the patient on a non-rebreather mask covered with a surgical mask (for obvious reasons). If the patient was able to maintain his current oxygen saturation, at least, we would cautiously proceed with the transport. If not, we would have an extremely low threshold for intubation. Our initial plan succeeded; the patient’s oxygen saturation remained in the high 80% range, and we started to move the patient over to our stretcher. That is when the first challenge to “my gut” ensued.
The Transport
As we were getting ready to head to the aircraft with our patient, we were met by the referring nurse, referring respiratory therapist, and the referring physician. They were all wondering why we were leaving without having the patient’s airway secured (I thought this to be an interesting question coming from an ED staff that could have arguably done this an hour or so prior to our arrival). As we explained our rationale to the physician and our interpretation of where the patient fell on the oxyhemoglobin dissociation curve, we could see our patient getting more anxious with a dipping oxygen saturation. I pulled the physician to the side, explained to him our plan if the patient decompensated while my partner calmed the patient’s anxiety. This allowed us to safely get the patient to the aircraft and continue the transport.
During our transport, the patient dropped his oxygen saturation to 82% with a mean arterial pressure (MAP) of 58, necessitating a 5-mcg push dose of vasopressin while a norepinephrine infusion was primed and initiated. Upon landing and offloading this patient, he stabilized with an oxygen saturation of 88%, a blood pressure of 90/58 (69) and he was breathing 30 times per minute. This was the best we had to offer upon hitting the doors of the COVID ICU.
As we entered the intensive care unit (ICU), we were again met with anxiety and an unwavering sense of urgency to intubate this patient. The ICU resident called for the airway cart, a stat page went overhead for anesthesia and our crew was being pushed to the side so that the team could rapidly move the patient from our stretcher to the ICU bed in preparation for an active resuscitation.
Luckily for everyone involved (including our patient), the ICU attending physician followed us into the room and put an immediate halt to the mass hysteria. He ordered a continuation of the pressor that we had initiated, a follow up chest x-ray, a STAT chest CT, and oxygen via a high-flow nasal cannula. When the resident questioned this rationale, the staff physician asked, “You have never seen a happy hypoxic?”
The Ridiculousness of COVID?
Over the past 8 months, words and phrases have been coined that if never spoken again, I would be completely content. “Social Distancing,” “Frontline,” “Essential Worker,” “ZOOM” used as a verb, and even “Quarrantini” in my opinion can’t make it to the Miriam Webster graveyard soon enough. However, of all of these terms (and I am just scratching the surface), the “Happy Hypoxic” has to be the most ridiculous to me. Having said that, I met my first “Happy Hypoxic” seven months following my initial COVID transport.
The term derives from those COVID patients in which there seems to be a disconnect between their profound hypoxemia and absence of proportional signs of respiratory distress. It is in historic contrast with what we have witnessed in patients with profound viral pneumonia in the past (my personal frame of reference being the H1N1 season of late 2009). As more is learned about this virus and how it contributes to critical illness, the respiratory pathology associated with COVID-induced pneumonia seems to be categorized into two phenotypes, each of which create their own havoc on different sides of the alveolar-capillary membrane.
The phenotype that most of us have seen and are used to is that of hypoxia with low lung compliance, non-cardiogenic pulmonary edema, and a significantly positive response to PEEP. This is the classic ARDS presentation that puts us in the historic mindset of ventilating “baby lungs” in accordance with the ARDSnet management strategy. These patients are less fluid responsive hemodynamically and their hypoxia responds more to our ventilator management.
The “other” phenotype (that I feel I may have experienced for the first time) is that of the normal to highly compliant lung. Tidal volumes / minute ventilation can be elevated, “recruitability” (i.e., responsiveness to PEEP) is minimal, and hypoxia is seemingly attributed to impaired regulation of pulmonary blood flow and ventilation-perfusion (V/Q) mismatch. This response is due to well-established pathology discovered in COVID patients including a propensity for microangiopathy, pulmonary blood clots, loss of regulation in lung perfusion, and maldistribution of blood flow.
Take Home Points
- While I am still skeptical with my “gut,” I would still advocate, at least, for allowing it an argument in any situation in which I can call upon it to help me with decision making (the experience that you already have certainly cannot hurt either).
- Without the luxury of a chest CT (something to quickly help identify the appropriate COVID-pneumonia phenotype), treat COVID-pneumonia like ARDS until the response to your interventions tells you not to (the information in which to make this decision shouldn’t take long to acquire).
- These patients did not read the ARDS text book. As Dr. Cereda so eloquently asks in one of the referenced articles: “Has critical care medicine evolved to the point where we are able to titrate care to the complexity of the disorder and the characteristics of individual patients?” These last eight months have taught me that the answer to whether critical care medicine has evolved should be an emphatic YES!
- There are two sides of the alveoli that contribute to gas exchange. If one side is not responsive, it probably isn’t a bad idea to give the other a look. I wish that I could say it was my astute clinical acumen and knowledge of the various COVID respiratory pathology phenotypes that helped me navigate my patient’s low oxygen saturation. But until I researched all of this post-transport, I was relying solely on my interpretation of basic physiology and I happened to “whack the mole” at the right time. Having said that, the response to patients with this presentation is clearer to me now.
References
Cereda, M., & Deutschman, C. S. (2020). Coronavirus Disease 2019 and Acute Respiratory Distress Syndrome: Why the Intensivist Is More Important Than Ever. Critical Care Medicine.
Dhont, S., Derom, E., Van Braeckel, E., Depuydt, P., & Lambrecht, B. N. (2020). The pathophysiology of ‘happy’hypoxemia in COVID-19. Respiratory Research, 21(1), 1-9.
Gattinoni, L., Chiumello, D., Caironi, P., Busana, M., Romitti, F., Brazzi, L., & Camporota, L. (2020). COVID-19 pneumonia: different respiratory treatments for different phenotypes?.
Gattinoni, L., Chiumello, D., & Rossi, S. (2020). COVID-19 pneumonia: ARDS or not?.
Gattinoni, L., Coppola, S., Cressoni, M., Busana, M., Rossi, S., & Chiumello, D. (2020). Covid-19 does not lead to a “typical” acute respiratory distress syndrome. American journal of respiratory and critical care medicine, 201(10), 1299-1300.
Mahjoub, Y., Rodenstein, D. O., & Jounieaux, V. (2020). Severe Covid-19 disease: rather AVDS than ARDS?. Critical Care, 24(1), 1-2.
Marini, J. J., & Gattinoni, L. (2020). Management of COVID-19 respiratory distress. Jama.