Getting ready to intubate? Let’s pray they don’t DESATurate!

You head over to bed 44 to meet the BLS crew as they start telling you about an 82 year old man who has been having trouble breathing and is “confused” as per his family.  His oxygen saturation when you check is 76% and quicker than you can say “sepsis”, the eager resident has popped the grey airway box open and is setting up to intubate.

You slap the NRB on and turn the O2 up all the way.  So why is the resident so focused on finding and placing a nasal cannula too?!

Apneic oxygenation (AO) is used to extend the time until critical arterial desaturation (SaO2 88-90%) following cessation of breathing/ventilation that occurs during intubation.  AO, similar to our other RSI preparation, premedication, and positioning, is used to optimize the patient prior to the first intubation attempt.

First demonstrated by anesthesiologists over 50 years ago, the alveoli of the lungs will continue to take up oxygen even in the absence of active breathing.  AO focuses on increasing a patient’s oxygen saturation through “nitrogen washout” in first the alveoli, and then throughout the circulation.  This effectively replaces the nitrogen one inhales in normal atmospheric air with oxygen and increases the patient’s overall oxygen storage in both the lungs (95% of a person’s natural reservoir) and bloodstream.  Maximizing pre-oxygenation provides us an additional buffer of time for “safe apnea” during oral intubation.  In a 2011 article in the Annals of Emergency Medicine, Weingart et al outline recommendations to reduce the risk of hypoxemia during emergency tracheal intubations which include emphasis on:

Pre-oxygenation for every patient

  • Nasal Cannula set at 15 L/min is the most effective method of AO
  • Non-rebreather mask at rates as high as possible
  • HOB elevated 20-30 degrees or Reverse Trendelenburg in suspected C-spine injuries
  • Minimum of 3 minutes total or 8 deep breaths, if possible

Take home:  Keep in mind the acronym “NO DESAT” which stands for “Nasal Oxygen During Efforts Securing A Tube”.  A nasal cannula with high flow rates should be placed on every patient prior to endotracheal intubation and left in place during attempts in order to reduce the risk of hypoxemia and deterioration.

Time for Terlipressin?

Correct, we don’t have terlipressin in the US, yet… Hopefully, sometime in the not so far off future we’ll have the chance to play around with it. Essentially it’s a synthetic analog of vasopressin which we are more familiar with. There’s some written about its use in variceal bleeds and here is a cool little study from Egypt using it for refractory septic shock.

They enrolled 80 ICU patients that were in refractory septic shock; meaning that they had to meet sepsis criteria and have the following three criteria:

  1. SBP < 90mm Hg or MAP < 70
  2. Received at least 1000ml of IVF or CVP 8-12cmH2O
  3. Necessitated more than 0.5 mcg/kg/min of norepinephrine

The 80 adult patients were split into two, pretty well matched groups, of 40. One group received adrenaline (0.2ug/kg/min) as their second-line vasopressor and the other group received a continuous infusion of terlipressin (1.3ug/kg/hr). This study was interesting because it only lasted for the next 6 hours after the second vasopressor was started. Unfortunately, they really didn’t look at patient related outcomes, but instead their primary endpoints were:

  1. MAP > 65 mmHg
  2. Systemic vascular resistance index > 1300 dynes s/cm5/m2
  3. Cardiac index > 4 L/min/m2
  4. Oxygen delivery index (DO2I) > 550 ml/min/m2

From an Emergency Medicine point-of-view the MAP is probably what we are most familiar with and is an easy enough measure to monitor in the ED.  After initially starting with a statistically equivalent MAP before the start of the second vasopressor, to having a statistically significant difference (p<0.001) after the 6 hours is hard to ignore despite the lack of reported clinical outcomes. This was in addition to showing improved hemodynamic measures and decreased doses of norepinephrine needed in the terlipressin group. This by no means is the do-all and end-all for terlipressin, and doesn’t mean we start throwing it at everything with hypotension when it gets approved in the US. Might as well get familiar with it now though, so when it does show up there are no surprises.

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Fixed dose PCC?

In the past, vitamin K and FFP were the mainstays of reversing warfarin, but now we have fancy new drugs like four-factor prothrombin complex concentrate (4F-PCCs).  4F-PCCs can rapidly reverse the INR of warfarin induced coagulopathy with less volume and quicker than FFP.  Many of the dosing regimens base the dose on the patient’s presenting INR and body weight, with ranges from 25-50 IU/kg.  A few problems arise with this approach, first the INR is not immediately available.  Second, 4F-PCCs are not cheap; costing up to $7,000 per patient in some cases.  Is there a fixed-dose regimen that we can give to patients on vitamin K antagonists without having to wait for the INR?

Some studies have looked at using 500 IU and 1000 IU fixed dose regimens for reversing the INR.  The 500 IU only corrected the INR in 43% of the patients, whereas the 1000 IU fixed dose study showed better clinical outcomes in 83.5% of the patients, but there is concern that the obesity epidemic in the United States will dilute the IU/kg concentration of the 4F-PCC and not be as efficacious.  Klein et al looked at using a fixed dose of 1500 IU of 4F-PCC for reversal of warfarin in 2015.  It was a relatively small sample of 38 patients on warfarin with the vast majority of them presenting with an intracranial hemorrhage.  Each patient had their INR drawn and then 1500 IU given before the result of the INR returned.  92.3% of the patients had their INR lowered to less than 2.0 after the 1500 IU of 4F-PCC and they reported no thrombotic events within the subsequent 7 days.  The presenting INR median was 3.3 (2.5-4.0) which was reduced to 1.4 (1.2-1.6) after administration of the 4F-PCC.  Additionally, this saved $40,273 dollars when compared to the typical INR and weight based dosing regimen for their patient sample.

We’ll have to figure out whether this fixed dose regimen of 1500 IU is the way to go, or should we base the dose solely on the patient’s weight and not worry about waiting on the INR.  Does waiting the extra 20 minutes for the INR lead to improved clinical outcomes?  And if we are going to start using a standard dose, is there a role for pre-hospital administration of the 4F-PCCs?

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Abdominal CPR?

There was a case report published in the Western Journal of Emergency Medicine last year about interposed abdominal compression CPR (IAC-CPR).  Personally, I’ve never heard anything of the sort and had to take a deeper look into it.  Essentially, you need two people to do compressions, one for the chest and one for the abdomen.  The abdominal compressor performs CPR with their hands about 5cm above the umbilicus and compressing about as deep as you would need to palpate the abdominal aorta pulse.  Both compress at the same rate and alternate their compressions; chest-abdomen-chest-abdomen and so on.  Theoretically, the abdominal compressor is acting as an external intra-aortic balloon pump.  By compressing the aorta during diastole, there is retrograde blood flow back into the coronaries.  Additionally, this abdominal compression increases venous return and promotes forward flow of the intrathoracic blood pool.  There have been no intra-abdominal injuries noted in survivors besides one pediatric traumatic pancreatitis reported in 1984.  The most recent review of IAC-CPR in Resuscitation showed significant improvements in the probability of achieving ROSC in the pre-hospital and in-hospital cardiac arrests when compared to standard CPR.  The question for me is why are we not doing this more? Is there harm in trying it if the person is already in cardiac arrest?

Post by: Terrance McGovern DO, MPH (@drtmcg13)