Felipe M.

Thank you very much Victoria and Grigori for your kind words!!!

And thank you very much as well for having joined me in this course and having supported it. It means a lot!

I hope you enjoy anaesthesia as much as I do, and wish you all the very best

Kindest regards

Felipe

Replying to Mark Laloo 13/07/2022 - 10:59

Hi there Mark

Urine retention related to trazodone is a side effect that is reported in humans, but I think there is not much in veterinary patients, maybe because it does not happen as often or because it has not been reported as much. After all, trazodone has only been administered in our patients since relatively recently.

Looking at the human literature, it seems this side effect is related to the central increase of serotonin concentrations (due to the inhibition of its reuptake) together with some anticholinergic effects.

So as you well say, absolutely. This could be a factor to be taken into account, especially in animals that can potentially already show some urinary retention. However as you say, if an IDUC is in place, it is not such a big problem. On the other hand, I would say that with the evidence we have to this date, I would still use trazodone regardless (unless urinary retention MUST be avoided -cystotomies, etc..-) and only stop it if we need to rule out causes for urinary retention, should it happen.

Excellent!

Felipe

Dear Emma

That is a very sensible plan actually! You can even increase your butorphanol to 0.4mg/kg and decrease a bit your alfaxalone to 1.5mg/kg IM. Sometimes with 2mg/kg animals can go totally anaesthetised. However not having seen the dog myself, I cannot recommend one or the other better since it depends on how you perceive the dog and whether you think you have a second chance to IM inject him/her! In any case, the combination makes perfect sense and I would use it too. Oxygen therapy, although basic in any sedation, will in this case help relieve some pressure on the right heart by vasodilating the lung. The clinical relevance of this is unknown since in normal conditions the pulmonary circulation is a low resistance/low pressure system anyway, but I guess that anything that helps is worth trying!

Giving some gabapentin and trazodone orally before the appointment is a great idea. The combination is also compatible with the sedation you describe. Just make sure you gauge the effect it’s had in the animal since any sedative will have at least additive effect and potentially even synergistic effect with both drugs. If the animal comes much calmer than normal, a lower dose of alfaxalone may work nicely already. Again, your judgement will be key here.

Very interesting case indeed!

Kind regards

Felipe

Hi there Emma

I hope you are well. I had a very lovely weekend thank you! Hope you did too. Thanks for the questions, they are very interesting questions indeed!

Let’s get them answered:

1.Even though a mini-lack anaesthetic circuit is an economical choice over a T-piece in regards to fresh gas flow, it does not have the ability to perform IPPV. So if we are thinking of patient safety, the ability to perform IPPV seems crucial. So when would you choose a mini-lack over a t-piece, and vice versa?

– It is a fantastic approach indeed how you are analysing your clinical choices from a patient safety perspective. This is how I try to focus all aspects of anaesthesia at the hospital, since patient safety is the most important part of anaesthesia. As you well say, a Lack breathing system (which is a Mapleson A breathing system) is much more economical than a T piece (Mapleson D) in terms of fresh gas flow used. And this is great from a economical but also environmental point of view. However as you say, a Lack (or a mini-Lack), does not allow IPPV. This is because the reservoir is at the inspiratory flow, and as soon as we give one or two ventilations, the reservoir is filled with alveolar gas. However, it does allow to give one or two breaths, should the animal need it. So I would say in absolute terms of safety, a Lack is AS safe as a T-piece in terms of what a breathing system is. But if the animal is for example apnoeic or requires mechanical ventilation, a Lack will be impractical and a different breathing system will be necessary (i.e. a circle, or a Mapleson D -T piece, Bain).
In terms of safety on the other hand, it is best to minimise breathing system swaps during an anaesthetic to avoid introducing factors that can lead to human error (wrong connections, valves closed), so planning ahead if the animal is likely going to need IPPV definitely makes sense. However if an animal happens to need IPPV during an anaesthetic, the breathing system can be carefully changed if necessary. As a side note, consider that a Lack breathing system can behave in a more or less similar way to a Mapleson D when high fresh gas flows are used (3-4 times minute volume). This can buy us time while using a Lack to ventilate, if the animal has transient apnoea or while we are setting up a different breathing system. I would generally recommend using this feature only temporarily. Another feature to bear in mind is that (depending on the make) many Lacks have an APL valve that when closed is totally closed, whereas a modified T-piece generally has a paediatric APL valve that will open even if closed, at a certain pressure (which we call an overpressure safety feature of the valve). So, with this assumption, maybe this does put things in favour of the T-piece but not due to the breathing system itself, because of the type of APL valve equipped (which I guess depending on the make of the Lack it could be also installed in it, so it’s really just a circumstantial advantage). So to sum up, both breathing systems are equally safe, but the Lack has the impracticality of not allowing IPPV. Safety depends on other things involved, including how we plan our choices and even what the suppliers equip different breathing systems with. But having said this, provided it makes clinical sense, a Lack is a very adequate and economical breathing system ( as an example, we use it instead of circles when a circle would not be used too often in the room, to avoid having dry soda lime).

2.When using a circle circuit, is it preferable to take the circuit you’ve been using through to theatre or have a new circuit already in there? Is there a safer/better option?

– Again, excellent approach to this. I have also given this a lot of thought in the past when building routines for everyday practice. And in this case I have a clearer answer! In my opinion, it is better to have a different breathing system waiting in theatre. The reason is that this way, you will have performed your machine check and checklist for your prep area before induction, and you will have done both things as well for the theatre machine. This means that both machines are checked, safe and that this is the routine you follow -making it repeatable-. On the other hand if the normal routine is for the breathing system to be taken through from prep, that will mean that the anaesthetic machine check in theatre will never be complete, since it will be left without a breathing system waiting for the other one to come through, This also introduces a source of complications/human error, which is the connection of a breathing system to the machine while an animal is connected to it. As an example, the breathing system could be potentially connected in an incorrect manner, especially if something is happening with the patient while moving through. For this reason, I always prefer to keep key transitions where complications or errors could occur as simple as I possibly can.

3.I also wondered if I could ask you about the use (or not use) of ALfaxan in cats with HCM. All of the cardiologists that I have discussed cases with are very happy to give Alfaxan to cats if needed to perform echos (if the cat is anxious normally they would give Butorphanol 0.2mg/kg IM and then ALfaxan (2mg/kg) IM) to allow echo. In lesson three you say that you would not be happy using Alfaxan with HCM due to the possible tachycardia as a side effect, therefore should I be avoiding Alfaxan when performing echos and if so why are the cardiologists happy using it? I hope that makes sense.

– Of course! It makes sense actually. Let me elaborate a bit to explain why I may have sounded inconsistent. Animals with HCM have a diastolic failure, which results in the incomplete relaxation of the ventricles in diastole and suboptimal ventricular filling (or end diastolic volume). As heart rate increases, diastolic time decreases, exacerbating this phenomenon. For this reason, we prefer to avoid too high heart rates in these animals. As I probably said in the video, a typical occurrence in theatre is that in a severe HCM, as soon as they show nociception and the HR increases, the BP decreases, which is counter intuitive (when compared to the healthy animal). For completeness, just a reminder that we also want to avoid too low heart rates as that can also cause a drop in cardiac output when the stroke volume is limited due by a diastolic failure.
Alfaxalone does not inhibit the baroreceptor reflex and allows the heart rate to increase as a compensation to the vasodilation during induction. However some animals show a very marked tachycardia, which in the animals at hand is undesirable. However there are a couple of things to clarify. This tachycardia does not happen in every animal (actually a marked tachycardia is much less common than an unaltered or just moderate increase of the HR), and in my experience, it is much rarer when the drug is administered IM as opposed to IV. These two factors, combined with the fact that alpha-2 agonists will greatly affect the measurements of an echo and that propofol is not suitable for IM injection, make the combination you mention a very sensible option (except in cases where any of the drugs could be contraindicated for any reason) for echo cardiography.
To be fair and to complete the background, in mild HCM I would quite likely be still happy to induce with alfaxalone. In moderate and cases I would definitely favour propofol, if adequate, to try to avoid tachycardia. Should propofol not be an option for any reason, I would potentially look at a co-induction with an agent that would decrease the amount of alfaxalone required to minimise the likelihood of tachycardia.
But just to emphasise again, one vital difference as well is the effects we usually see when given IV versus those when given IM.
I hope this makes all sense!

Very interesting stuff.

Excellent!

Felipe

Hi there Mark

Great question actually.

Rapid sequence induction is actually a human term that describes the administration of a pre-calculated dose of anaesthetic plus a neuromuscular blocking agent. In human anaesthesia usually the induction agent is only used to cause loss of consciousness (when we stop communicating or counting backwards) and then a NMBA is administered to relax the larynx and intubate the trachea. In veterinary anaesthesia we are fortunately able to get away without NMBAs for intubation, but it means that we rely more on the anaesthetic agent to facilitate muscle relaxation too.

When RSI is used in veterinary context, it usually means the administration of the anaesthetic agent at a set dose in a fast fashion, so as to gain airway access fast. This is the choice sometimes in cases like: high risk of regurgitation, oesophageal or gastric obstructions, constant vomiting, hypersalivation, obesity, upper airway obstruction, among others.

The technique is used to gain rapid airway access and avoid problems like aspiration or obstruction, but is a trade-off with titration of the agent, as you say. However, when a RSI is needed, usually it is the best option for the animal in the big scheme of things. Side effects of the induction agent like apnoea and cardiovascular depression may be more apparent, but usually their importance in these animals is lower than the ongoing airway risk and therefore the latter is addressed first.

Pros: fast airway access and protection, ability to control ventilation faster.
Cons: no titration of agent, potentially more side effects from higher dose, less pleasant induction if pre-anaesthetic medication is not a possibility, complete dependency on anaesthetist as all airway reflexes are abolished fast, need for rapid airway control, need for all equipment and staff to be ready (these last two are more a requirement than a con)

So all in all, if we are a bit literal, what we do in veterinary anaesthesia is more a modified RSI (mRSI) at best as we do not give a NMBA. However the purpose and the effect is similar indeed.

In terms of drugs, propofol or alfaxalone are very adequate. Ketamine I would say is not a preferred agent if an alternative is available as the onset is slightly longer.

Co-inductions (which will also be covered in the course!) many times are overall slower in nature due to more than one agent being administered. Also we need to consider what we need the co-inductor to do for the patient and if it is then justified to introduce it as a factor. If the co-inductor is fentanyl for example, the animal could lose ability to effectively control the airway after it, hindering us taking control as the inductor has not yet been administered. If the co-inductor is midazolam, it is best given after an initial dose of inductor agent to prevent agitation and disinhibition, therefore not serving the purpose either as it will increase the induction time. Ketamine does not seem to fit the profile since its onset is longer than propofol and we will be dealing with delayed effects or having to wait, which defeats the purpose. The only one I could possibly be happy with is lidocaine, which can be given with the animal totally awake and will not cause sedation (therefore “the clock has not started ticking” for us to have to rush to gain airway control) but once the induction agent is given will blunt the cough reflex to some extent -if this is what we need-. However in the case of lidocaine, the animal needs to be stable before induction so that the time to administer the lidocaine is justified. In general terms, when considering doing a mRSI in a patient, we usually do not want to be dealing with many drugs and benefit from having a simple plan of action as we will be dealing with the airway in a very fast sequenced manner.

So in summary, yes, we will likely see more side effects from the induction as a titration is always preferable, however when we choose to implement an mRSI, it is because the benefits offset the aforementioned side effects.

I hope this helps!

Excellent!

Felipe

Replying to Idris Vandekinderen 19/06/2022 - 21:43

Hi Idris

Thank you so much for the kind words! I am very happy you are enjoying the course.

That is a good point actually, let me clarify:

Both nasal prongs and nasal cannulae are methods of providing oxygen therapy to patients who need it. In anaesthesia, oxygen therapy is often administered by mask, as it is usually temporary (pre-oxygenation, recovery…). However, in some animals, longer term oxygen therapy may be needed (animals with respiratory disease, thoracic surgery, very slow recovery…). In these cases, we tend to change method on to something which is a bit easier to wear for the animal, even if moving a bit in the kennel. This is where nasal prongs and nasal cannulae play a massive role.
In my experience, nasal prongs (the clear tube with two outlets that sit on the nose and just go in less than a centimeter) are used when the oxygen dependency is only mild. Nasal prongs can achieve reasonable FiO2 (being realistic, in a dog, around 50% perhaps and of course this depends on flow administered), however they do not sit perfect in many dogs due to the design being human (which explains why the actual FiO2 is lower than in humans). Patients can also remove them easily with just sneezing, which can result in de-stabilisation of the condition. On the other hand they can be placed easily in an awake animal with minimal stress, which makes them many times desirable.
Nasal cannulae are tubes inserted inside the nasal cavity up to (I always recommend a bit less) the medial canthus of the eye. They are there secured to the animal with staples or suture. Because of this they are much more reliable as they tend to stay in place much better, so it’s much less likely to allow an animal to pull them out (although it can happen…). They can be placed unilaterally or bilaterally, and the FiO2 can be as high as 77%, depending on flow of course. This tends to be the choice for animals with moderate oxygen dependency, and usually they are placed before recovery from anaesthesia as the placement is a bit uncomfortable as is securing it to the animal. The placement and the fixation does require of a bit more experience, and as a technique it is more invasive.

Both are very valid options and play different roles in our clinical experience.

I hope this helps!

Excellent!

Felipe

Replying to Sarah Fiddy 11/06/2022 - 12:14

Hi Sarah

Thank you so much for your kind words, I am very glad you enjoyed it! Right, let’s get these interesting questions answered:

– I really like the idea of having oxygen cylinder for recovery in kennel, but if this is not possible, how long would you recommend giving oxygen post operatively? And how long should you administer oxygen via the ET tube once the anaesthetic has stopped? I try to keep the o2 going for a 2-3 minutes then switch the iso off until the animal is ready to extubate – is this ok?

I would recommend administering oxygen until the animal is clearly conscious and looking fairly recovered, for example able to move or hold their heads and responding to stimuli. If monitoring SpO2, which I would recommend in recovery, I give oxygen until the animal is consistently maintaining a SpO2 of 97% or more on room air for 3-5 consecutive minutes.
To provide oxygen, should piped oxygen not be available in kennels, the oxygen cylinder is very handy but there are other options. For example, recovering the animal in theatre using the anaesthetic machine to provide oxygen. Alternatively, if this gets too much in the way of the workflow, a splitter Schrader can be connected to the oxygen pipeline socket or to a J cylinder, which will allow us to have a second connection to oxygen. In this one we could connect a “bubbler” humidifier with a flowmeter with a “green” oxygen tube that can be used for flow by or mask oxygen therapy. Please note this latter system does not have a valve and should NEVER be connected to an ET tube.
After the isoflurane has been stopped, I usually keep them connected for a couple of minutes on just oxygen or if you have gas analysis, until the ETISO reads 0. Then I disconnect them and keep them on flow by by holding the breathing system close but not connected to the ET tube, or I take them to recovery and administer oxygen there. I do this while monitoring SpO2. If the animal is consistently saturating above 97% on room air, for 3-5 consecutive minutes, I am happy to stop the oxygen.
On the other hand, if you prefer to discontinue the isoflurane and keep them connected to just oxygen until ready to extubate, that is totally fine too! Just ensure you are very quick in spotting the cues for extubation to avoid having movement of the head while still connected and an accidental self-extubation which can cause damage.

– I try to titrate induction agents to effect slowly over a few minutes but sometimes still see apnoea – what is the best way to manage this? A nurse I once worked with blew down the ET tube which worked but I guess not recommended! In these cases I usually turn the iso off and given breathes until the animal starts to breathe by themselves.

This unfortunately happens to all of us every now and then! A strategy to prevent this, especially if alpha 2 agonists are on board or if cardiac output is low, is to have pauses of 20-30 seconds every time we reach 0.5-1mg/kg increment in the dose of propofol or alfaxalone, in order to give it time for us to see the full effect of it, which can take much longer than anticipated. Still, it can sometimes happen regardless. When we see apnoea, all we need to do is to manually support the ventilation by giving a breath every 5-10 seconds whilst keeping a close eye on the pulseoximeter to ensure the saturation does not drop (if it does, we will need to increase ventilation and ensure we are providing oxygen and that we have airway control). After a couple of minutes, the animal will begin breathing again (when the plasma concentration of the induction agent has dropped a bit). We can give some pauses to our ventilation every now and then providing SpO2 is above 97%, to give the animal a chance to start breathing spontaneously (by allowing PaCO2 to increase).
I cannot personally see a reason to blow down an ET tube and I cannot recommend it due to health and safety reasons as well as the lack of control of how much pressure and volume we are putting in the airway, therefore risking volutrauma and barotrauma. Ventilating manually using an anaesthetic breathing system is much safer for yourself and the animal, and as a plus we will be providing oxygen too, rather than room air!
I usually do not stop the inhalant anaesthetic if post-induction apnoea happens, as by manually giving breaths with oxygen and inhalant means that when the animal resumes spontaneous ventilation, the anaesthesia depth will be good due to more stable amounts of inhalant in the alveoli, rather than getting light when they start breathing by themselves until the inhalant concentration builds up. Of course this depends a lot on how deep the plane of anaesthesia is in the animal after induction. If you assess it as too deep, then waiting a bit until starting the inhalant is a sensible idea so as to not make the animal any deeper until the injectable anaesthetic has redistributed a bit.

– You mentioned briefly about not giving medetomidine to paediatric patients and I wondered the reason why and what you would prefer to use instead?

Excellent topic! We will go in more depth in subsequent sessions, but in the meantime… Paediatric patients have an immature CV system up to 3 months of age (depends a lot on each animal), which means that the contractility is somewhat fixed, and therefore the cardiac output is very heart rate dependent. By giving alpha 2 agonists we will be increasing the afterload via vasoconstriction (at the beginning), which will difficult the cardiac work. They will also cause bradycardia, which will have a direct negative effect on cardiac output in these animals. For these reasons, it is best to steer away from them until they are older than 3 months of age (again depends a lot on the animal).
Other options are an opioid only pre-anaesthetic medication, or if very young (in the first 2-3 weeks) considering adding midazolam (0.1-0.2mg/kg IM/IV). Unfortunately, midazolam sometimes has the opposite effect, causing excitation and disinhibition. When using an opioid only, methadone (0.1-0.3mg/kg IM/IV) is a good option, but alternatively, pethidine (2-4mg/kg IM administration only) usually gives a better sedation than methadone, albeit having a shorter analgesic effect.

I hope this helps!

Excellent!

Felipe