I really do read your mail. I know sometimes it seems like I don t, but that s because often it takes me a while to get my head around an issue. Part of the problem is that you ask difficult questions. Ask me to write a column comparing the Justice League to the Super Friends, and I ll have the answer to you in an hour. EMS questions take more time.
Such was a question posed a while back by Ryland Kendrick of Fairfax County, Va. Concerned about the administration of drugs through an endotracheal tube, he s discovered a conflict between the proper fluid volume to allow adequate drug dosing and the risk of “drowning the patient” in the carrier fluid. Pragmatically, he notes that no matter what volume of fluid you give, most of it seems to come back up the tube. What s a medic to do?
This was a tough issue to consider because a host of problems are involved. To explore this fully, issues of endotracheal drug effect and efficacy and of the site and mechanism of drug delivery must all be reviewed. Just thinking about it, I have no doubt why I ve put off writing this column. But it s time now, and I can t stall any longer. Pull up a chair, grab a donut, and pour a cup of tea. This may take a while.
Assumptions
To examine these questions in any brief format, we need to share a few assumptions. The first is that certain drugs administered via the endotracheal route cause a physiologic effect. This is undoubtedly true, and a review of the literature finds this proposition so well accepted that there is very little new work addressing this point. In the context of our discussion, clinical effect simply means that the drug does something.
The second assumption is that clinical efficacy is different than clinical effect. Clinical efficacy means that the drug does what you want it to do. Ideally, these are one and the same thing. If a patient s blood pressure rises when you give epinephrine, the drug has a clinical effect. If it can raise the patient s pressure enough to prevent hypoperfusion of vital tissues (the goal of giving the drug), then it also has clinical efficacy.
Although all the ACLS “NAVEL” drugs demonstrate a clinical or physiologic effect when given via the endotracheal tube, the question of efficacy (at least in theory) remains in doubt. There is little work comparing survival rates (the ultimate test of efficacy in cardiac arrest) of patients given drugs via the IV or ET route. So we consider effect as equivalent to efficacy, which is not such a bad leap to make. But even for those agents in whom clinical efficacy (in our broader sense of the word) has been noted, the effect does not result when an equivalent IV dose is given down the ET tube. The effect is seen only when much larger doses are administered.
The 2000 ACLS Guidelines are surprisingly brief in their discussion of endotracheal drug administration. In adults, the guidelines indicate that epinephrine, lidocaine and atropine can be given down the tube. Doses should be 2 to 2.5 times the IV dose and should be diluted in 10 cc of fluid. (The question of whether to mix a solution of drug in an additional 10 cc of fluid, or simply bring the total volume of solution up to 10 cc, is not addressed.) These dosing recommendations are complicated by pediatric guidelines suggesting that the optimal drug doses for endotracheal administration are unknown. Studies indicate that epinephrine should be administered at 10 times the normal dose, and it is “logical to assume” that doses of other drugs should also be increased. Although these advisories are confusing, I don t think they represent any crucial physiologic differences between adults and kids. I think it reflects the lack of literature on the subject and honest differences of opinion.
The one message that seems clear is that endotracheal drugs don t work too well. To get anything out of them, you ve got to get a lot of it in.
Dead space
The key question here is why a drug that works well when given IV does not provoke a similar, dose-equivalent, response when given endotracheally? The most likely culprit is simply anatomy. The reason we don t often give IM medications in the field is that the blood supply to large muscle tissue is relatively sparse, and drug absorption is delayed. The same is true of drugs administered via the ET route, and the key is to look at the concept of respiratory “dead space.”
“Dead spaces” are those areas of the respiratory tree where no effective gas exchange takes place. Gas exchange occurs at the level of the alveoli and the microcirculation (capillaries). It does not occur in the pharynx, larynx, trachea, mainstem bronchi or other higher divisions of the respiratory tree. The respiratory “dead space” is not an insignificant volume. In young adults, this space can represent 150 cc of total lung capacity. Dead space volume increases slightly with age.
In the intubated patient, the tube also occupies dead space. A volume of fluid must not only traverse this space, but also migrate past the carina and into the smaller airways to have any chance of absorption into the pulmonary veins. Which finally leads us to a series of experiments I ll simply call Mr. Wizard s Revenge.
My five-year-old son may beconvinced that I m older than dirt, but there are some things I m not grizzled enough to remember. One of these is a 1950 s television show called “Watch Mr. Wizard.” In this science show for kids, Mr. Wizard (a.k.a. Don Herbert, still alive and well at the stately age of 86) would demonstrate the grand principles of science using ordinary household objects. While this may sound tame by today s standards, the show was quite influential in its time. “Mr. Wizard sent this country to the moon,” notes Bill Nye, the Science Guy.
(Speaking of the cosmos, it s been said that the first form of contact aliens will have with us is through our radio and television waves, which have been screaming through space at the speed of light. I hope they first get to know us through Mr. Wizard. It s more likely they ll think every earth male is a Cuban bandleader shouting “Babaloooooocy!” My fear is that they ll find reruns of “Mr. Ed” and “My Mother, the Car.”)
Inspired by Mr. Wizard s inspiration, I decided to find out just how much fluid you could get into an endotracheal tube. Maybe, I thought, that was the whole problem with the back flow and why endotracheal drugs don t work. Maybe they just couldn t get through the tube.
It turns out that if you straighten and then occlude an 8.0 endotracheal tube (recall that 8.0 refers to the internal diameter of the tube in millimeters), it will hold 17 cc of fluid. However, airways are very rarely straight. They bend in an anterior fashion, inducing a very gentle 30-degree curve along the length of the tube. If you consider that the bend in the tube as it comes out of the package is similar to the bend on the tube when placed in the airway, a full 15 cc of fluid can fit into the tube before it drips out the eyelet at the end of the channel. Note that most prepackaged ACLS drugs (such as epinephrine, atropine and lidocaine) come in 10 cc vials, and you can already see that the fluid volume will have a hard time exiting the tube.
I mentioned that you can get 15 cc of fluid into an 8.0 endotracheal tube without overflow. If you try this yourself, you ll find that this is only true when you place the fluid into the tube very slowly, to avoid turbulent flow and splashing. However, that s not how we give ET drugs. Just for fun, I took the same ET tube, blasted in 10 cc of water via an 18-gauge needle (the same as found on the premixed vials) as fast as I could and measured the remainder. Only about 12 cc were left in the tube. Some of it came out the distal end, but most of it came out on my hand. A quick look at the tube as I pushed the fluid showed the effects of splashing, of piling additional pressure (in the form of more fluid) upon fluid that, in turn, is fighting atmospheric pressure. So it seems like 10 cc is not enough fluid to even get the drug out of the tube; and the act of rapidly pushing ET fluid, rather than the capacity of the endotracheal tube itself, is what causes backflow.
(Being a fan of Monsieur Poiselle, I also wondered if the problem of backflow might be related to the diameter of the tube. Were we trying to push fluid through tubes that could not handle the volume? Not having a flow meter of any kind, I tried an experiment using a syringe, a needle and a little math. I took at 20 gauge needle, hooked it to a syringe and timed how long it took to push 20 cc of fluid through this with my thumb as hard as I could. It turns out that 20 cc of high-pressure flow through a 20-gauge needle, with an internal diameter of 1.27 mm, took 6.71 seconds to accomplish. Doing the math, one might surmise that for an 8.0 mm endotracheal tube, the equivalent 20 cc flow at the same pressure would take much less than a second. Clearly, there s no problem here. Even in a pediatric size ET tube, the ability of the tube to permit flow should not be a problem; a 4.0 tube should allow 20 cc of flow in two seconds or less. There may be an issue with neonatal ET tubes, in that one might allow up to 10 seconds to push an ET agent through a 2.0 tube. From an everyday practical standpoint, however, flow and backwash of drug given through an ET does not seem related to tube size at all.)
My brief amateur foray into the investigative realm indicates that although gently administering the fluid will get the entire volume into the ET tube, it will not get all the way through the tube (especially in our prepackaged 10 cc doses). Injecting fluid into the tube under pressure seems to only enhance splashing, fluid turbulence and backwash. So the solution would seem to be to find a way to get a larger volume of fluid (enough to fill the channel and spill out the distal end) under relatively low pressure into the tube. The fact that studies document an enhanced effect of ACLS agents when given in larger volumes provides pharmacologic support for this claim.
Alas, it s not that easy. When fluid under low pressure spills out the end of the ET tube, it spills into the trachea just above the carina. It s still in the respiratory dead space, where minimal gas exchange and drug absorption occur. We need to find a way to get the drug deeper into the pulmonary tissue, to the sites of maximal drug absorption. This is one of the reasons for “pushing” a drug in solution down the ET tube. As the fluid is pushed and flow becomes turbulent, air is introduce into the mixture, and the added pressure causes droplets to form and be expelled out of the tube. The pressure at which these droplets are expelled force them farther down the respiratory tree, presumably to where the drug can be better absorbed by the body. The smaller and lighter the droplets, the father they can progress into the respiratory tract. Injecting fluid at a higher pressure through an ET tube can enhance droplet formation and decrease droplet size. However, we ve discovered that when we inject fluid into an ET tube under pressure, most of what we get is backflow. And while we re on the topic, remember that the fluid molecules with the endotracheal tube are often quite happy to be adherent to one another and to the side of the tube. When this surface tension is broken by air being pushed through the channel, the resulting droplets do not form in a steady, uniform manner, but spring from the pool of fluid residing in the tube as larger, heavier “glops” which are poorly conducted throughout the respiratory tree.
(Do you like the scientific term “glops?” Truth be told, I just don t know what else to call them. But think of them as the well, “glops” of fluid formed if you try to blow a bubble of water off the roof of a just-washed car. The surface tension of the water molecules, and their tendency to adhere to the roof of the car, manifests the breakup of the water bubble as irregular beads “glops.” OK?)
Before we get too carried away with fluid dynamics, it s important to note that there s a component of respiratory mechanics that prevent us from getting good drug absorption down the ET tube. Consider at what phase in ventilation we administer ET drugs. We give the patient a good breath, unhook the bag, and try to push the drug. We do this at the same time that the elastic recoil of the chest is trying to push air back out. Even when we continue to aggressively bag the patient to force the fluid into the tube, between each breath there is a mechanical expiration. Is it any wonder that much of our drug comes back to use, bubbling up the tube with the air that really wants to leave?
Here s what we re left with. In order to use a drug via the ET route, we need a relatively large volume of solution placed into the respiratory tree under low pressure. We need droplets of the fluid to form as small as possible to penetrate the pulmonary tissues and to avoid the mechanical disadvantage of elastic chest recoil and expiration. How do we accomplish this? Tune in next week for the answer.
