Over the last decade or two, we have all seen, read, and are hopefully now doing some interesting stuff with the A in the ABC’s. Here, we discuss three interesting topics involving ventilating critically ill patients using less breaths…sometimes way less…sometimes not breathing at all.
Part 1
For starters, we all know that the better we oxygenate our patients before intubation, the more time we have before they start to desaturate. This is fairly common sense. Less common sense is the idea of apneic oxygenation. Though perhaps not intuitive, numerous studies [1] have demonstrated prolonged oxygenation with high flow nasal cannula even when the patient is not breathing! Apparently, the oxygen diffuses down to the alveoli in enough concentration to improve the PaO2. So, now we all (hopefully) put a nasal cannula on all our patients before and during intubation.
Part 2
Then we discovered the concept of permissive hypercapnia. You see, asthmatics/COPD’ers ventilator settings MUST be set differently than the usual.
What vent settings should you use for your asthmatics?With a high I:E ratio or low RR, the patients CO2 rises and pH drops…but they do better. There are case reports of extreme measurements (one with pCO2 375 and pH 6.6 and full recovery![3,4]) but I could not find clear guidelines for specific pH and pCO2 levels. Special note: I:E ratio is a setting on the vent that refers to the Inspiratory time:Expiratory time.
Extra Special note: Leaving any patient on 100% FiO2 is entirely unacceptable. Your goal should be O2sat 92-95% with PaO2 200-300. If you doubt me, ask Dr. Ashika Jain and she can fill your head with illuminating knowledge (or you can read the reference).[2]
Part 3 But in Trauma?!
First off, multiple studies have shown that trauma patients intubated in the field do worse [4,5,6]. In our own NYC, BLS units (NOT ACLS) are called for trauma and a “scoop and run” approach is recommended. Though there are many possible reasons for this, such as simple delay in time to OR and hemostasis, one concern is that intubating trauma patients causes harm. How could that be you ask?
Let’s talk physiology! When you intubate you take a system built on negative pressure (ribs move out, increasing intra-thoracic volume, which decreases pressure per PV=nRT), and turn it into one of positive pressure (ribs move because air is being pushed in). The increase in intra-thoracic pressure makes it more difficult for venous blood to return to the heart.
Onto the review [8]:19 pigs divided into three groups. All sedated, put on propofol drip and fully lined (A-line, CVL with Swan-Ganz catheter, and line into carotid artery). One group was oxygenated with a facemask, another intubated with manual breaths though an ambu bag, and the third was given manual breaths through a bag-valve mask. After 10 minutes of “equilibration time”, baseline lab values and vital signs were recorded. Then they opened up line in the carotid artery to model hemorrhagic shock.
The results: No statistical significant time to death (all around 50 minutes). The NRB group had higher CO2, lower pH, higher bicarbonate, higher cardiac output, higher CVP, lower lactate, lower creatinine, and decreased hypothermia. Base excesses were not statistically different in the three groups.
The discussion:
While animal studies are clearly not practice changing, it does raise some interesting points, but, it depends on how you look at it. The authors conclude that: positive pressure ventilation does not improve survival in severe hemorrhagic shock. PPV does cause decreased pCO2 levels, but worsens many other surrogate markers (lactate, creatinine, temperature). They recommend more studies.
I found this study interesting for a few reasons.
1. They conclude that PPV does not improve survival. Firstly, the pig is not dying of a respiratory problem, it’s dying of a not enough blood problem. There shouldn’t be a survival benefit to intubation. Oddly, I would think that PPV would decrease short term survival secondary to the physiologic changes discussed above. Even with worse labs/vital signs/temperature in the PPV group, mortality, the actual outcome we care about, was unchanged. One concern not brought up in this paper is the decreased risk of aspiration in intubating patients unable to protect their airway.
2. It was interesting to me that the intubated group became more hypothermic – theoretically secondary to cool/dry air bypassing the upper respiratory tract and being pumped into the lungs. Here, one of the lethal triad in trauma is increased by BVM and intubation! Although the clinical significance of 37.5C to 35.5C in a trauma patient otherwise not being warmed is of questionable significance – lesson here: do not let your intubated trauma patients go hypothermic.
3. I already agreed and continue to agree with this paper’s conclusion that there is definitely no need to intubate trauma patients in the field in urban environments.
4. Though not mentioned, it does throw a little mud on ATLS. I mean, A-B-C right? Well, here the bleeding pigs died equally fast no matter what you did to A. ACLS has already changed to C-A-B, will ATLS? Or does it just take a smart physician to decide large volume, continued blood loss may need to be addressed before the airway.
To Conclude
Here are three prime examples of when the “A” doesn’t matter.
1. Put a nasal cannula on every patient before and during intubation
2. Use permissive hypercapnea when intubating an asthmatic or COPD’er.
3. Do NOT put the vent at 100% FiO2 and walk away.
4. Focus on what the hemorrhagic shock trauma patient immediately needs – blood (and maybe a NC or facemask).
By Dr. Andrew Grock
Special thanks to Dr. Adam Aluisio and Dr. Shira Grock for their invaluable input.
References
[1] Scott D. Weingart, MD, Richard M. Levitan, MD Preoxygenation and Prevention of Desaturation During Emergency Airway Management. Ann Emerg Med. 2012 Mar;59(3):165-75.e1. doi: 10.1016 [2]Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K, Parrillo JE, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010 Jun 2;303(21):2165-71. doi: 10.1001/jama.2010.707.[3] Hickling KG, Walsh J, Henderson S, et al. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med 1994;22:1568–1578
[4] Potkin RT, Swenson ER. Resuscitation from severe acute hypercapnia: determinants of tolerance and survival. Chest 1992;102:1742–1745 [5] Cudnik MT1, Newgard CD, Wang H, Bangs C, Herrington R 4th. Distance impacts mortality in trauma patients with an intubation attempt. Prehosp Emerg Care. 2008 Oct-Dec;12(4):459-66. doi: 10.1080/10903120802290745.
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