Reader Responses

Myron Yaster MD

I received several reader responses to the Cricoid Pressure PAAD. Here is a sample…

James J. Thomas:

This is the difference between superstition and faith. I love it. Science isn't the truth. It seeks the truth. If science changes its mind, it wasn't lying, it just got better information. 

Diane Gordon

I find that my practice aligns with several of the more current guidelines – applying cricoid pressure in situations where it might be useful but removing it if it is impeding visualization of the glottis for intubation. I think an important consideration in the United States is litigation and legal exposure if pulmonary aspiration does occur. Surely there are myriad expert witnesses who would testify that cricoid pressure should have been used, despite there being no certainty to that statement. I counsel my trainees that I use cricoid pressure in rapid sequence intubation and document it thus mostly to show that I was concerned about the risk of aspiration and that I’m doing everything that might prevent it. I have no hesitation to remove cricoid pressure if the view of the glottis is not satisfactory during intubation. I’d be interested to hear about closed claims database  data regarding litigation for pulmonary aspiration complications and expert opinion on whether using cricoid pressure decreases legal exposure risk. 

Elliot J. Krane

Thank you for bringing up this interesting and fascinating topic.  I am always pleased when longstanding medical myths fall, and there have been so many of them since we were trained.  However I’m not so confident that cricoid pressure should be assigned to the dustbin of history.  Yet.

It is clearly the case that inexpert cricoid pressure can obstruct the airway, push it to one side or another, make laryngoscopic view of the airway impossible, and it is equally the case that in most cases of non-fasted patients it is not really useful or necessary.  However, in my view there are still cases in which it is not just indicated but mandatory.  Unfortunately (or fortunately), these cases are infrequent enough that no RCT will demonstrate its usefulness, these cases are just buried in a lot of statistical noise.  

There is in my mind a big difference between the non-fasted patient who eats some breakfast before an 8:00 case, and has hours to empty the stomach before induction while the parents drive them to the hospital and they spend 2 hours in preop, or the infant who breast feeds an hour before induction, and the patient with (1) a pregnancy at term, (2) a small bowel obstruction with feculent matter in the stomach, or (3) a patient with a gastric outlet obstruction who has eaten. I’ll share an anecdote of a hen’s-tooth rare case that illustrates:

There was a very conservative anesthesiologist at Seattle Children’s who always played everything by the book.  He was so conservative he flossed his teeth in the locker room after lunch.  So, there came to the OR a young woman of about 10 or 12 who had a colon esophageal interposition for esophageal atresia years before. Several times a year the suture line of the distal colon esophagus strictured, the colon esophagus filled with food and fermented over a few days, and she would come to the OR for dilatation. She was a resusci-Annie for RSIs.  

Our colleague performed a classic RSI with his resident, and he applied the cricoid pressure.  In spite of this her colon esophagus passively emptied a liter of fermenting food into her oral cavity and she aspirated.  Case cancelled.  Two hours later she was dead from gram negative sepsis. Sadly, this case occurred on the colleague’s last day of clinical practice before retiring. What a way to exit the stage!

The lesson here is that a colon esophagus does not pass under the cricoid cartilage, it is under the strap muscles of the neck.  Who would have thought of that?  The point is that regurgitation of gastric contents or food can be lethal, and in fact was once the most common cause of mortality when general anesthesia was used to deliver babies, as you know.

So yes, Smith is right (c and d), CP can shift the anatomy right or left if not carefully applied with gentleness.  Ahmed’s paper (e) is meaningless, who cares that 68% of respondents do not believe it is useful?  Allen (f) is right, cricoid pressure IS difficult in babies.  (In babies it is probably less necessary, aspiration of breast milk from the stomach is probably quite benign).  And the Cochrane database certainly is correct that there have been no RCTs of CP and there never will be.  Neither are there RCTs of the efficacy of parachutes in sky diving, to quote an old saw.

The point is that aspiration of foul material / acid can be lethal or lead to severe lung damage. But it’s rare.  So do we abandon a procedure that may be important 0.05% of the time?  Does anyone die from CP?  No.  (Well, only if the CP applier is too stubborn to relax it if the laryngoscopist cannot see bupkis.) Or do we perhaps change the indication from all RSIs to those with clear risk factors?  But let’s not throw the baby out with the bathwater!

Right to left shunt and speed of induction

George Politis MD

There are a few things in today’s cardiac themed PAAD that are incorrect. First, the statement regarding patients right to left shunts that said the slowest induction time was for volatile anesthetics with lower solubility is incorrect. It should say that the slowing of induction caused by right to left shunts is most pronounced for the least soluble anesthetic agents (and least pronounced for more soluble agents). Less soluble volatiles are still going to have an overall faster induction; ether is not going to suddenly win the induction race with sevo just because there is a right to left shunt, but an ether induction with a right to left shunt will still look like an ether induction without a shunt (snail like) while a sevo induction will be noticeable slower (but would still run circles around ether). Second, the explanation for why inductions are slowed by a right to left shunt, which states that less anesthetic is taken up by the lungs and therefore less reaches the brain, is not correct. The model in the diagram in the PAAD shows that 2 L per min flow is going to the lungs when there is no shunt, while with right to left shunt there is 4 liters a minute retuning to the heart, two liters per minute shunted right to left, leaving 2 l per minute still going to the lungs. Uptake therefore remains the same, but the admixture of blood that heads systemically is a mixture of volatile poor blood returning from the body and volatile rich blood from the lungs, and the result is a lower volatile arterial partial pressure heading to the CNS.
If that doesn’t make a tremendous amount of sense to you, here is what I wrote about this topic for Bruno (Bissonette’s) pediatric anesthesia textbook:

Anesthetic Uptake: Effect of Ventilation Perfusion Mismatches and Shunting at the Cardiac Level
An increase in the ratio of ventilation to perfusion (V/Q) occurs when there is ventilation of unperfused (dead space ventilation) or under perfused alveoli. Increases in V/Q do not alter the rate of rise of FA/FI as long as arterial CO2 remains normal because the overall increase in ventilation necessary to maintain normocarbia also maintains the ventilation of perfused alveoli at normal levels. On the other hand, decreases in V/Q which occur with segmental pulmonary disease such as atelectasis or pneumonia (pulmonary right to left shunting) or with cardiac right to left shunting do have a substantial effect on anesthetic partial pressure rise. Decreased uptake of anesthetic leads to a faster rise in FA/FI. However, arterial partial pressure rise is slower because the end mixture of blood returning to the left heart is diminished by blood that had not passed ventilated alveoli. The result is a gap between the alveolar and arterial partial pressures, which is indicative of right to left shunting. A minor amount of right to left shunting and mismatch is present in healthy individuals, and anesthesia has long been known to exacerbate that mismatch.[23] Larger mismatches are pathologic and slow anesthetic induction. Slowing occurs to the greatest extent with the least soluble anesthetics, and the reason is as follows. In order to maintain normocarbia in the face of a right to left shunt, overall ventilation is increased, which increases ventilation to areas of normally perfused lung. As noted above, more soluble volatile anesthetics are most able to augment their rate of rise of FA/FI by increasing alveolar ventilation, and in this case they do so in the regions of the lung that are over ventilated and normally perfused. Therefore more soluble anesthetics maintain an end mixture of blood returning to the left heart that has an arterial anesthetic partial pressure close to that expected without shunting.[11]
Left to right shunts have different effects than right to left shunts. Normally, with left to right shunting, cardiac output is increased so that systemic tissue perfusion is maintained at normal levels. In that case, the amount of mixed venous blood returning to the right heart ready for anesthetic uptake is normal. There is no effect on alveolar anesthetic uptake by the shunted saturated blood, and therefore no change occurs in the rate of alveolar partial pressure rise. However, if cardiac output is not increased, and peripheral perfusion is not maintained then there will be less anesthetic uptake at the lung, and a more rapid rise in alveolar anesthetic partial pressure but a slower rise in tissue partial pressure. The anesthetic effect is therefore delayed.