This EM-Critical Care Medicine case presentation focused on a very complex resuscitation with multiple facets. The case is notable because it includes most, if not all, of the factors we should consider when worrying about a peri-intubation arrest. Let’s recap the initial case and apply what was learned in conference about how to manage it. (Note, while this is a real case presentation, the subsequent management is fictional.)
You are working the end of a long CCT night shift, and as you are taking a walk to shake off the dust, you get a notification from EMS:
“Obese, male, rapidly breathing with profuse sweating.” ETA: 5 minutes
Being the smart resident you are you round up your team and prepare for some initial interventions:
- A team – you notify the nurses, attending, and your junior to be at the ready
- To get the patient plugged in, lucky for you, a bed in trauma 1 is set up and you have an open monitor ready to go
- Access: you hand your junior phlebotomy equipment and pray they don’t stab themselves
- Your respiratory resus equipment: a hypoxemic patient means you are definitely going to need to deliver O2, probably with ventilatory support, and then try to fix the underlying respiratory problem. For your initial weapons, you should consider = non rebreather +/- additional nasal cannula, a back up BVM ready to go (given obesity may want to anticipate the need for a peep valve now)
- More advanced support equipment based off your gestalt: obese, hypoxic, and the fact that EMS has already used CPAP, it is very reasonable to anticipate and notify respiratory to get a BiPAP ready and waiting by the bed. (For this patient, most experienced clinicians would probably start here.)
The patient is brought in and he looks to have BMI well over 40. The paramedics report that upon their arrival he went into respiratory failure (SpO2 83% on room air) so they started CPAP. They gave him epinephrine IM and albuterol/ipratroprium via nebulizer. He is talking a few words through the CPAP mask; you hear poor air entry b/l; pulses are palpable and rapid. You ask to transfer him over to the stretcher, get him on the monitor, start a peripheral line, and continue him on BiPAP. His initial vital signs show RR: 38/min, BP: 86/69 mm Hg Temp: 98.9 F SpO2: 100% bedside glucose 248 mg/dl.2) While transferring the patient over, respiratory asks for BiPAP settings. EMS had this guy at a CPAP of 5 cm H2O. How are you going to set his BiPAP?
I know that many of us like “10/5” and FiO2 titrated to level of hypoxemia, but there are some more advanced settings to play with based on specific patient considerations.
Even though this patient has hypoxemic respiratory failure, you should anticipate some degree of obesity hypoventilation syndrome (OHS) given his size and therefore suspect that he’s going to require some increased EPAP. It is not uncommon to have OHS patients on settings like 25/20.
(Not sure exactly how to set a BIPAP or titrate the settings? No problem – check out this podcast: http://www.aaem.org/UserFiles/media/aaem-critical-care-episode-11.mp3 )
You are a little nervous about dropping his BP further, so you decide to start at IPAP 10 cm H2O/EPAP 5 cm H2O and will ramp up based off respiratory effort and tidal volume
(For a full review of hypercapneic respiratory failure, specifically the use of high IPAP and EPAP in OHS check out the BTS guidelines: http://thorax.bmj.com/content/71/Suppl_2/ii1)
Given his reported hypoxemia you decide to start on 100% FiO2 and will titrate down to the lowest level the patient can tolerate. Lucky for you, at 10/5 he is “pulling” volumes of about 400 mL and his respiratory rate goes down to about 25 breaths/min.
You give him dexamethasone, magnesium, and additional albuterol to treat a possible asthma/COPD exacerbation and send off your labs. In this case, the differential diagnosis is very broad and so it is reasonable to check a CBC for WBC SIRS criteria. The patient is vomiting and slightly altered, so electrolytes, LFTs, and kidney function are reasonable. Additionally, acid- base status is going to become very important as we will see shortly. A venous blood gas is usually sufficient. However, in cases of hypercarbia, arterial blood gas will give a more accurate PCO2. We also want to check a lactate (to quantify degree of shock) so either arterial or venous shock panel should be ordered.
(Shameless plug for our blog – a post on ABG vs VBG: http://blog.clinicalmonster.com/2016/09/vbg-reliability-hypercarbia/ )
You start a liter of NS on pressure bag (assuming some insensible fluid loss) to try increase his BP/perfusion.
You obtain more history from the brother: 36-year-old male with past medical history of dyslipidemia, DM, HTN, and schizophrenia. He had been feeling ill for the past month with almost daily nausea and vomiting but refused to seek medical attention. Earlier this morning, he was walking from the bathroom and complained to his family of shortness of breath. As he was talking, his brother saw him slump against the wall for a moment and briefly lose consciousness. He was diaphoretic at the time. He was guided to sit on the floor, and EMS was called. Additional history was unobtainable. A quick physical examination doesn’t add very much other than revealing that this large gentleman also has a short neck and a small jaw.
You go to bother chest xray and grab your sono for a quick bedside ultrasound. ECG is ordered but not yet done. At this point, your nurses grab you because the patient is getting less responsive. You assess the patient, and he is now very sleepy and breathing agonally. Repeat vitals show that his hypotension has not responded to the fluid bolus.At the same time, you get a call from the lab for critical values – what wonderful timing:
PaCO2: 31.7 mm Hg
PaO2: 76.3 mm Hg
Bicarb: 3 mEq/ L
Cr 16 mg/dL
K 8 mEq/L
It is apparent this gentleman is not doing well on the current BiPAP settings. Despite initially responding to 10/5 and FiO2 100%, he is now tachypneic to 35/minute and taking in tidal volumes of around 200 mL (hypopneic). You suspect that even if you optimize his settings again, he will need mechanical ventilation. His blood gas only complicates things showing a mixed respiratory and metabolic acidosis (yes, an ABG would be ideal and you should do Winter’s formula here). There is also renal failure with hyperkalemia.
3) Because you read FOAM all the time, there are some things that trigger you to realize this will not be a straightforward rapid sequence intubation (RSI). What are they?
Hypotension, hypoxemia/ potential to desaturate, acidosis (PH)
In terms of predictors of a potential peri-intubation arrest, the greatest LR+ belongs to hypotension (specifically SBP < 90 mm Hg).
Resuscitate before intubating.
You choose a triple attack.
- For hypoxemia:
The patient should be upright to unload some weight off of the chest and minimize work of breathing. You should continue BiPAP to optimize oxygenation/ denitrogenation. You should also reoptimize your settings. You supplement with 100% FIO2 for now and titrate up to IPAP 20 and EPAP 10 as described above. Higher EPAP may drop his BP more, but you are now going to address that directly.
2. For the hypotension:
You need to move quickly to secure this airway, and the patient has already failed to respond to a fluid bolus. In a world of limitless time, you might check fluid responsiveness by doing a straight leg raise. However, in this critically ill patient who is also being positive pressure ventilated, you decide to start norepinephrine so that it’s running (it can be done peripherally at this stage!) by the time you intubate. Though, mentally, you might feel the urge to address the hypoxemia first, starting pressors is a definite rate-limiting step and your nurses will need time to mix and hang the bag (allegedly 5 minutes if the medicine is in the ED and readily available). While the infusion is being prepared, you play with BIPAP and positioning. If you need to move even quicker it’s probably a good idea to use push dose epinephrine or phenylephrine.
See this post for thoughts on when to use push-dose epi vs starting a drip:
3. For the acidosis:
This is a slightly more insidious problem. Let’s recap: this patient has a mixed respiratory and metabolic acidosis (ph 6.9) and renal failure with hyperkalemia. We know that acidosis is one of the reversible causes (an “H”) of cardiac arrest as it will reduce cardiac contractility. Though we don’t have a bedside sonogram to confirm, it is reasonable to assume that reduced cardiac contractility may be contributing to his hypotension. He may not be fully compensating through hyperventilation (do the math: his PaCO2 should be 10.5 mm Hg to 14.5 mm Hg and instead it is currently 31.7 mm Hg). So, how do we address this?
The most important thing to remember is that any apnea is going to make his PaCO2 rise, worsen his acidosis, further reduce cardiac contractility, and possibly lead to cardiac arrest. For now, we have temporized this by decreasing his work of breathing and hopefully increasing his minute ventilation with BIPAP. But, we must keep this in mind for later when we intubate and put the patient on the vent. Another temporizing measures we can do is give bicarbonate. Although its not a long-term solution – the patient is in respiratory failure he will not be able to breathe off the CO2 generated from the infusion – it may raise his pH temporarily and give us some “wiggle” room (i.e. prevent cardiovascular collapse during sedation for intubation). What this man really needs to correct the severe metabolic acidosis is hemodialysis. You start the bicarbonate infusion, page renal stat, and treat the deleterious cardiac effects of hyperkalemia with IV calcium.
The nurses scramble to medicate this patient. You take one deep breath and prepare to intubate.5) How are you going to optimize this intubation so it’s a life-saving procedure and not a nail in the coffin?
TL:DR the lit review:
Avoid drugs that will drop BP – ketamine is your friend here.
Patients in shock often have impaired consciousness so you can give ½ dose sedative
“Roc rocks” and “succ sucks”. This obese patient who is already hypoxemic has potential to desaturate very quickly. With rocuronium, there is more time before desaturation and [theoretically] less risk with patients who have hyperkalemia.[3,4] However, there is the risk of cardiovascular collapse with giving any paralytic. Remember the above discussion about acidosis? Making the patient apneic for any period will worsen respiratory acidosis and puts him at increased risk for cardiovascular collapse from critical acidemia! Also, if giving a paralytic, it’s important to know that in a patient with shock, the drug may not get where it needs to go as easily. If you are going to give it, make it a double dose .
You do not “have to” do a rapid sequence intubation, and there is a growing body of literature for delayed sequence intubation (DSI) – giving the sedative first to aid in preoxygenation/denitrogenation and then giving the paralytic later once you are ready to intubate. What is the logic for this? The short version is that delirious patients in extremis often fight pre-oxygenation. Giving a sedative/ paralytic combo and then “bagging” is not ideal for these patients. In our example, the patient is taking rapid shallow breaths (about 200 mL x 30 breaths/minute). Some amount of this may be psychogenic. If we can calm him down, we may be able to greatly increase his minute ventilation (by increasing his tidal volume). This should also help tremendously with his hypercarbia!
Here is a link to DSI central: https://emcrit.org/dsi/
Obese, short/fat neck, small jaw?
This dude needs to be in sniffing position. Stack sheets under his upper back and head now so that when he lays back he will be in an ideal ear to sternum position.
P.S. here’s a cool EM:Rap on sniffing vs ramping and the original paper:
Make sure you have them. Choose what you are comfortable with.
In this gentlemen glidescope, bougie, LMA, and cricothyrotomy kit should be right next to you. Do not be afraid to have anesthesia available.
Although the patient is somnolent, he is tachypneic and hyoponeic, so you give ketamine to try to assist with non-invasive ventilation. After your temporizing measures, the patient is breathing at 24/minute at tidal volumes of about 400 mL (about twice his previous minute ventilation). His SaO2 has been at 100% for about 5 minutes. He is appropriately denitrogenated and ready to be intubated.
You feel comfortable that your preparation has momentarily stabilized the patient, and considering the likely difficulty of intubation, you decide to maximize your chance of first-pass success with a paralytic.
This is a difficult consideration. Succinylcholine is not an ideal choice because of the theoretical risk of exacerbating the hyperkalemia. Any paralytic is scary because of his severe acidemia. You have to balance the risk of cardiovascular collapse from paralytic (in this case rocuronium) vs. the risk involved in a prolonged difficult intubation for which rescue will not be easy (this patient would also be very difficult to “cric”). There is no right answer here, and each clinical situation will be different. The important thing to know is that there are options. You can try to optimize the patient as best as possible and do a DSI. You can also try intubating without a paralytic (sedation-only intubation) so that the patient can ventilate during the intubation. There is also the option of awake intubation.
In this hypothetical scenario though, you made the right call. After giving calcium and starting norepinephrine and bicarbonate infusions, the patient’s hemodynamics improved. You adequately preoxygenated/denitrogenated him with BiPAP, and with airway positioning and medications, you use video laryngoscopy (so that your nervous attending can look on) and intubate him successfully on the first attempt. You set your vent to “hyperventilate out” this acidosis, and now that you have a pressor on and blood pressure is improved, you ramp up the PEEP to a level where there is more optimal lung compliance. An example of settings might be tidal volume 450 mL (6-8 cc/kg ideal body weight), PEEP 10 (consistent with previous BiPAP setting and for the OHS), respiratory rate 30/min, and FIO2 100% (you can go down later). Congratulations! Renal is on their way to dialyze him, and he has a bed in the MICU. You may now go home and go to sleep…. after you write all your notes.
- Know your predictors of peri-intubation arrest and difficult airway.
- Whenever possible, resuscitate your patient with all of the various tools available to you before you intubate. Specifically, remember and address all of your “HOP Killers”
- Ketamine is your friend; hypotensive patient gets ½ dose sedative and double-dose paralytic (if you are going to give it).
- Optimize the glottic view with ideal positioning, equipment and back up plan.
- Remember post-tube management: keep that pressure up, optimize your vent, and get definitive treatment for the underlying problem.
I’d also like to add that this particular topic has been covered extremely well in the FOAM ED world and for a more comprehensive review of the management, I would suggest visiting:
1. Kim WY, Kwak MK, Ko BS, et al. Factors Associated with the Occurrence of Cardiac Arrest after Emergency Tracheal Intubation in the Emergency Department. Chen X, ed. PLoS ONE. 2014;9(11):e112779. doi:10.1371/journal.pone.0112779.
2. Effects of changes of pH on the contractile function of cardiac muscle
H. Orchard, J. C. Kentish American Journal of Physiology – Cell Physiology Jun 1990, 258 (6)C967-C981;
3. Taha, S. K., El-Khatib, M. F., Baraka, A. S., Haidar, Y. A., Abdallah, F. W., Zbeidy, R. A. and Siddik-Sayyid, S. M. (2010), Effect of suxamethonium vs rocuronium on onset of oxygen desaturation during apnoea following rapid sequence induction. Anaesthesia, 65: 358–361. doi:10.1111/j.1365-2044.2010.06243.x
4. TANG, L., LI, S., HUANG, S., MA, H. and WANG, Z. (2011), Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients. Acta Anaesthesiologica Scandinavica, 55: 203–208. doi:10.1111/j.1399-6576.2010.02365.x
5. OHS patients may need higher PEEP to keep their lungs open against all their weight.