Neuromuscular blocking agents are used daily. As a reader of this blog you know that my views are unorthodox. Even iconoclastic! The opinions that I express are not what board examiners expect an examinee to regurgitate. In no way, am I suggesting that mine are methods that other anesthesiologists should use.
I post here to communicate with my residents the thought processes that I employ when doing anesthesia. In this blog it is how I use muscle relaxants.
If possible I use inhalation anesthesia only. TIVA is not in my lexicon unless inhalation agents and muscle relaxants can not be used for a particular operation.
1. I use muscle relaxants for most cases (even when a muscle relaxant is not necessary, (e.g., for an ankle operation that can be done with inhalation agent alone). I use vecuronium exclusively and usually not more than 5 mg at the start of any operation. Muscle relaxants are useful to keep the patient from coughing/moving before the depth of inhaled anesthetic is adequate. After induction, many patients (especially older patients) are hypotensive owing to the absence of surgical stimulation. Paralysis allows for continuing with low (amnesic) concentrations of inhaled anesthetic so as to minimize hypotension.
2. I use only Fentanyl and in amounts less than 250 ug. This will ensure that the respiratory center will not be too depressed and that there will be respiratory efforts when the muscle relaxant is wearing off. Stay with me here.
3. I keep the EtCO2 around 40 torr. This is necessary for respiratory drive and respiratory efforts when the muscle relaxant is wearing off.
With minimum narcotic on board and the EtCO2 at 40, respiratory efforts, indicated by a so-called “curare cleft” (a notch in the plateau at the end of the EtCO2 expiration wave form) signal that the muscle relaxant is wearing off.
For me, respiratory effort is the best indicator of the degree of neuromuscular blockade. Respiratory effort (continuously displayed on the EtCO2 monitor) requires no special monitoring equipment. Twitch monitoring is notoriously confusing and faulty. They depend too much on proper electrode placement, which are often not properly located, as well as battery power, which is rarely checked and is often inadequate.
4. Once respiratory efforts start, I decide whether to continue administering vecuronium or not. I usually don’t administer more relaxant in cases where relaxants are not necessary for the operation (ankle/foot surgery). For intraabdominal operations and other operations that require muscle relaxation, I continue administering vecuronium in 1-2 mg amounts depending on the estimated duration of the remainder of the procedure.
This is my way of dosing and it is my equivalent of always having “1 twitch in the train of 4” but without the using a twitch monitor.
By now, I am depending on the the inhalation agent, increments of Fentanyl to maintain adequate anesthesia, and muscle relaxant to keep the patient from moving.
5. At the end of the procedure, I try to have the patient breathing spontaneously or with pressure support. This is feasible if the inhalation agent, Fentanyl, and muscle relaxant have been dosed as described above.
6. The next decision is whether muscle relaxant reversal is necessary or not. For this, I monitor the Tidal Volume (TV) and Minute Ventilation (MV). If the patient has adequate TV and MV, and a normal EtCO2 waveform, I don’t reverse the muscle relaxation. If the TV and MV are inadequate or curare cleft still present, then I give glycopyrrolate and neostigmine.
I know! Miller’s text book and recent articles in the journals say that in order to prevent residual paralysis, all patient should have their neuromuscular blockade reversed. I disagree. Glycopyrrolate and neostigmine are not benign drugs. So, why give them if they are not necessary?
Almost all operations take at least an hour (taking into account prepping and draping, and closure of the skin). Five mg of vecuronium given immediately after induction and not re-dosed is unlikely to cause significant paralysis at the end of an hour.
See blog post: Do not wait for twitch return after succinylcholine
It is my opinion and practice not to reverse at this time if the TV, MV, and EtCO2 waveform of the spontaneously breathing patient are adequate. Inadequate TV, MV, and presence of a curare cleft, obviously requires reversal.
OK! Is there any evidence that I might have a clue as to what I’ve posted here?
Take a look at this figure.
Generally speaking, most drugs have their action terminated by redistribution away from the effector site to peripheral compartments. Some of a 5 mg dose of vecuronium has its effect at the neuromuscular junction (NMJ) but some of it is also distributed to peripheral sites. As redistribution continues molecules that disassociate from the NMJ are sequestered by other tissues. This is what terminates a small dose of vecuronium. This is the situation above, that is not likely to require reversal.
Continued dosing with vecuronium, will prolong its action because the peripheral compartments will become more saturated and make them less capable of sequestering any vecuronium that dissociates from the NMJ. This situation will require reversal.
Another way to look at this is shown in this figure.
This figure shows the elimination of 0.2 mg/kg of vecuronium (14 mg in a 70 kg patient). Ignore the blue curve that is taken from patients with cirrhosis. After the vecuronium is injected into the circulation, its concentration in plasma decreases rapidly at first and then more slowly. The shape of this curve is divided into an initial (distribution) phase and a terminal (elimination or metabolism) phase.
A similar curve for 5 mg of vecuronium, as I suggest above, will have a lower peak and the curve will be shifted to the left. This small amount of vecuronium will be terminated and eliminate more quickly and not likely require reversal.