Let's discuss a common misunderstanding: when to use intermittent positive pressure ventilation (IPPV)), how much to use, when and how to stop assisting a patient's ventilation.
Let's discuss a common misunderstanding: when to use intermittent positive pressure ventilation (IPPV)), how much to use, when and how to stop assisting a patient's ventilation. This can be administered by hand, manual IPPV, or by a machine, in which case we call it mechanical IPPV. I raise this issue in light of recently hearing the often cited, but completely misconstrued "don't breathe for the patient or the patient will not breath for themselves. Just let carbon dioxide accumulate." True, under non-anesthesia condition. False, under anesthesia. One can let carbon dioxide accumulate until the proverbial cows come home. If our anesthetic agents tell the brain not to take a breath as frequently as the patient would when awake, then we need to help them breath. Simple! The advantages are that breathing for them will make them equilibrate faster to the number on the isoflurane dial. When we are finished breathing for them on pure oxygen will help them to arouse and extubate. If we do not breath for them, they will likely have some degree of respiratory acidosis, experience mild to severe acidemia, and possible accumulate enough carbon dioxide in their blood to cause an injury. The downside is we have to focus on our patient to avoid iatrogenic injury.
The quickest summary is to give an example of how these misunderstanding hurt veterinary patients is that insufficient ventilation causes respiratory acidosis, this leads to patient acidemia. Our medications and inhalant agents SUPPRESS the normal drive to breath. The way to see if one needs to apply IPPV is to read a capnograph. When the patients’ need a manual breath or need a ventilator, it will require them until the medications have been discontinued and been metabolized. There is rational and straightforward way to stop breathing for the patient, same as manually or mechanically. Wait until the effects on the patient that dulled his ventilatory drive have left his system.
Let's run through a case example. Bear, is an aptly named healthy 6-year-old 33 kg chocolate Labrador retriever is premedicated with hydromorphone and dexmedetomidine, both IM. After Bear vomited and became sedate, a catheter is placed in his right cephalic vein and he is induced with midazolam and ketamine. He is intubated and placed on 2% isoflurane delivered in a circle system using 2 L/Min oxygen. He is clipped, prepped and received a morphine-saline epidural for his stifle surgery. He is moved and instrumented on the capnograph in the OR. There is no waveform, so his technician gives a breath, makes a nice "elephant holding the tail" waveform and the ETCO2 is 68 mm Hg. The seasoned staff reaches across and indicates that she should stop, because "he won't breath for himself if we keep breathing for him" so she stops. Because her employer is wonderful, and the patient is stable and large, she practices her art line skills on the tiny artery under the front paw and uses a point of care machine to test the acid base status. There she recognizes that the patient's pH is 7.2. He is spontaneously ventilating, but he has sharp little peaks that read 45 mmHg and few deep breaths. Bear’s technician gives Bear a breath, achieves that rectangular waveform and now his ETCO2 is 72 mmHg. What should she do? Ignore the seasoned tech and breath for the patient? If so, why? If she starts breathing for the patient, how will she stop, and will it delay his recovery? She has had enough education to know something is not correct, but not enough experience to figure out what to do or how to rationally explain why she FEELS breathing for the patient is her best choice, and no idea when to stop IPPV.
The answer is that she should breath for the patient. She is recognizing these peaks represent less than full exhalations or air escaping as the surgeon manipulates the stifle for the procedure. To start breathing for the patient of this size, she starts by checking the cuff on the ETT tube is full and closes the pop-off valve (adjustable pressure release valve) and inflate to a patient airway pressure of 15 or 20 cm H20, then opens the pop off valve again, watching his thorax rise and fall under the drapes. She starts googling "pop off occlusion valve" to make this process more streamlined. She begins with breathing every 10-15 seconds and assess if the ETCO2 can be brought down to approximately 45 mmHg. She continues this until there is a chance to discontinue the isoflurane. After that happens, she rouses the patient by continuing to breathe for the patient on pure oxygen. One can pause and see if Bear is ventilating on his, but then return to ventilating for Bear if he has not lightened his plane of anesthesia. The more frequent and full the breaths, the faster the isoflurane will be offloaded and exhaled into the scavenging side of the circle breathing system. Bear will wake up faster than if he had been left to breath room air on his own sluggish ventilation. In his medicated state, he could again fail to breath enough to keep his carbon dioxide levels at a healthy level. Bear could even have two reversal drugs, atipamezole and flumazenil if he failed to ventilate himself to a safe carbon dioxide level within a reasonable amount of time. But he does not need it.
Bear, still on oxygen, wakes up, opens his eyes and lifts his head. He is extubated and lays back down on his gurney. The surgeon comments that she doesn't smell isoflurane as strongly as usual. She's correct, Bear was exhaling into the scavenging system for a while. Everyone was happy. The pop-off occlusion valve and prep room capnography machine are ordered because the employer is so generous and helpful.
Next article, Bear goes on the ventilator for his other stifle surgery. How do we "wean" him off that apparatus, and when? What are the impacts on blood pressure and how do we balance them for short-term anesthesia ventilation?
During anesthesia, we frequently find ourselves working hard to keep the patient in a delicate balance between a plane of anesthesia deep enough to prevent movement or perception of pain but yet not so deep as to obliterate the homeostatic mechanisms keeping the patient perfused, ventilated, and oxygenated. What signs in the patient tell us that they are in a plane of anesthesia that is insufficient for a procedure, i.e. “too light,” or a plane that is too deep to be compatible with life, i.e.“too deep”? See Table 1.
The visual and tactile inquiries that the anesthetist can easily make in most procedures are to check the jaw tone, eye position, and palpebral/corneal reflexes. The exception is when a pet is purposefully paralyzed with neuromuscular blocking agents. Otherwise, an anesthetist can monitor the strength required to gently open the jaw. A tight jaw generally means a pet is in a lighter plane of anesthesia than a loose jaw but there is no “absolute value” for this measurement that ensures the correct plane of anesthesia. An anesthetist should open the lids and examine the eye position. In brief, the eye position begins with the iris centered, and then moves, ventromedially, towards the medial canthus as the plane of anesthesia deepens, and then moves back outward with a dilated pupil if the animal is too deep. If the animal is emerging from anesthesia, the iris returns to its normal centered position and is constricted or normal. Other useful information is gained from the palpebral reflex, is diminished or absent (not always, especially when using injectable anesthetics such as ketamine) and the corneal reflex should always be present., Monitoring jaw tone and eye position at set intervals and at the initiation of a painful stimulus is easy can give the anesthetist useful information, in addition to blood pressure, heart rate, respiratory rate, and end-tidal carbon dioxide (CO2). This can aid the decision-making process.
Next, we consider a case example. Patient: 6 month old intact female yellow Labrador retriever in good health. Presents for OVH, Premedication: hydromorphone 0.1 mg/kg IM, dexmedetomidine 0.005 mg/kg IM, glycopyrrolate 0.01 mg/kg (not given). Induction and intubation: Propofol 4 mg/kg to effect. Maintenance: Isoflurane 2% and LRS @10 ml/kg/hr
At about 45 minutes post-premedication, the anesthetist notes that the patient’s heart rate, respiratory rate, and blood pressure have risen. The anesthetist considers that the medetomidine may have been eliminated, or the surgical stimulation has increased, and the patient is now “too light” and may need a higher concentration of inspired isoflurane to maintain a surgical level of anesthsia. Before turning up the vaporizer, she checks the jaw tone and finds it to feel tight. She notes the iris of the eye appears to be returning the center of the orbit, as previously the iris was only partially visible at the medial canthus. She checks the end-tidal carbon dioxide monitor and notes the dog has hyperventilated herself to a 30 mm Hg of carbon dioxide. This confirms to her that the patient is “too light” so she increases the patient from 2% to 3% of inspired isoflurane.
For a while, her patient seems perfect:
Blood pressure: mean = 70 mmHg, Jaw tone: loose (but not too loose), Respiratory rate: 15 per minute, End tidal CO2: 45 mm Hg, Heart rate: 80 bpm, Eye position: ventromedial, Palpebral: decreased,Corneal: intact
The anesthetist is asked to retrieve a surgical pack. When she looks at the monitor again, she sees that the heart rate is now at a new peak and the patient is taking many frequent, shallow breaths. Her first instinct is to think “the patient is still too light” but before she increases the isoflurane concentration again, she checks the jaw tone and finds that it is looser than before and that the iris is again only partially visible at the medial canthus of the eye.
Blood pressure: mean = 40 mm Hg, Jaw tone: very loose, Respiratory rate: 60 per minute, End-tidal CO2= 60 mm Hg, Heart rate: 120 bpm, Eye position: central with dilated pupil, Palpebral absent, corneal intact
The anesthetist decides the patient is instead, “too deep” and she reduces the concentration of inspired isoflurane and assists ventilation. The heart rate returns to normal and the respirations become less frequent and deeper. The parameters return to baseline
Summary: In this case, the rapid heart rate could be attributed to the body’s compensatory mechanism for a falling arterial blood pressure or an elevated level of carbon dioxide, or both. The rapid respiratory rate was a response to the high end-tidal CO2 measurement, which reflects a high arterial blood content of CO2 in the healthy dog. In this case, the respiratoand heart rate by themselves could have misled the anesthetist to increase the % of isoflurane delivered to the patient and caused harm to the health of the patient. By considering all the available information, from both electronic monitors and hands-on examination of the patient, the correct next-step was taken. By integrating jaw tone and eye position assessments into your anesthesia practice, one can improve the safety of anesthesia and prevent a common mistake of assuming that a rapid heart and coupled with a rapid respiratory rate is always a sign of a “too light” plane of anesthesia.
Assessing Anesthetic Depth in Patients Anesthetized with Isoflurane:
Corneal reflex (if very very deep)
End-tidal Carbon Dioxide (spontaneous ventilation)
Assessment: Lighter plane with tachycardia, tachypnea, High blood pressure, jaw tone present or increased normocapnea or hypocapnea;Palpebral reflex Normal with eye rolled central and nystagmus Intact corneal reflex
What do you do? Increase isoflurane or add analgesic medication(s).
Deeper plane can have: tachycardia or bradycardia, Tachypnea or bradypnea or apnea, Low blood pressure, Jaw tone decreased or absent, Central, dilated pupil. Lost palpebral, eye position staring straight at you, ETCO2 is >50 mm Hg. Tachycardia can follow hypotension, eventually this leads to bradycardia as plane deepens
Assessment: deeper plane
What do you do: Reduce isoflurane, assist ventilation, increase IVF rate, ±-pressor agents (hypotension), ±anticholinergics (bradycardia)
Acceptable plane is defined as follows:
Normal heart rate
Near normal respiratory rate
Blood pressure Mean >60 mm Hg or Systolic >90 mm Hg
Jaw tone neither loose nor tight
Slow palpebral or none
Central or ventral, normal pupil size
Intact corneal reflex, but don't check it unless one has to because of damage to corneal.
Normal or slightly elevated; Supplement ventilation as required.
 Chapter 2, Lumb and Jones’ Veterinary Anesthesia and Analgesia, 4th ed.,
 Chapter: 2 & 6 (Box 2-1, 2-2, 2-6, 6-4), William W. Muir III. Anesthesia and analgesia: a guide to canine, feline, and exotic animal practice, 2nd ed. For VCA Animal Hospitals.
Question: How do you safely anesthetize a patient with abnormal vascular circulation and changes on echocardiograph examination?
What are the consequences of the different premedication or intravenous anesthesia drugs? How and why would you choose one inhalant over another? What intra-operative concerns could you anticipate based on
the procedure and what drugs could be used to prevent or address this consequence?
Answer and Discussion: To safely anesthetize a patient with compromised cardiac function and abnormal circulation, the goal is to preserve the function as close to the non-anesthetized normal parameters as possible. A premedication of fentanyl and midazolam, followed by induction with etomidate or alfaxalone and maintenance with sevoflurane and a combined fentanyl and midazolam constant rate infusion can be used. Etomidate is a cardiac-sparing induction agent that is rapidly hydrolyzed by both hepatic and plasma esterases.12 The drawback is that it can suppress the adrenocorticol responses and cortisol for 2-6 hours. An alternative to etomidate is Alfaxalone which gives a smooth induction with minimal cardiac impact.
Injectable premedication drugs that are considered cardiac-safe include benzodiazepines and opioids.3 The main negative cardiac effect that manifests with opioids is a decrease in heart rate because of the stimulation of the medullary vagal nucleus resulting in increased vagal tone.4 This can be corrected with an anticholinergic such as glycopyrrolate.5 Benzodiazepines, such as midazolam, have minimal impact on cardiac function and act synergistically with fentanyl. 3
The choice of sevoflurane as the inhalant agent was made because of its innate characteristic of being poorly soluble in blood, less so than isoflurane. The advantage is that the lower the blood solubility of an anesthetic agent is, the more rapidly the partial pressure can be changed and the faster the degree of CNS depression can be adjusted.6 This translates into a faster induction, faster recovery, and a faster rate of adjustment of the anesthetic depth.
The potential problems with this regimen are an opioid-induced bradycardia treated with an anticholinergic and resulting in a sinus tachycardia. This can negatively impact perfusion and make intrathoracic suture placement more difficult. A consideration for this procedure was that the ligation can increase the blood pressure and cause a reflex bradycardia or arrest. In some cases, we use repeat boluses of glycopyrrolate to correct a low heart rate.
Using the correct breathing circuit and oxygen flow rate:
Most veterinarians and veterinary nurses are aware of the two different types of breathing circuits: non-rebreathing circuits and the circle system. The circle system is the most often used but sometimes it is not the best solution to the problem of maintaining adequate ventilation under anesthesia. To expand on this topic, let us consider forces that impair ventilation (surgical position, anesthetic drugs, endotracheal tubes), what tools we have to support ventilation (different sized breathing circuits, positive pressure ventilation either manually or from mechanical means) and how capnography fits into this discussion.
My opinion is that allowing an animal to ventilate spontaneously is preferable to positive pressure ventilation. But there are important caveats to that statement, the main one is that if the spontaneous ventilation is not sufficient to clear carbon dioxide and provide oxygen transportation to the tissues, we need to interfere. So why do we not always put every animal on a ventilator? Reviewing the physiology in brief, the pressure inside the thoracic cavity is negative at rest and more negative upon inspiration. This serves well to inflate the lungs. When the lungs inflate, they actually improve the pulmonary circulation and therefore enable respiration, filling the alveoli with gases and increasing the size of the capillary vessels by traction. The correlation to this is that the venous return, via the vena cavae to the right atrium of the heart, termed “preload” is also enhanced by this negative pressure. Positive pressure ventilation, just like the name implies, pushes air into the lungs and changes the intrathoracic pressure from negative to positive and therefore reduces the preload to the heart. This is not a benefit to the animal and how well this is tolerated is multifactoral. In summary, cardiac output gives us an idea of perfusion (with systemic vascular resistence which is another newsletter), and cardiac output depends on preload (need to put blood into the heart to get more out to systemic circulation) and positive pressure ventilation decreases cardiac output. How do we relate cardiac output to the veterinary patients? We frequently think of part of the equation, the mean arterial pressure. Positive pressure ventilation causes lower mean arterial blood pressure than spontaneous ventilation, with all other factors being the same.
To avoid interfering with spontaneous ventilation, we choose different size breathing circuits for different patients. The non-rebreathing circuits, such as the Mapleson D, the Bain (a coaxial modification of the Mapleson-D), the Ayres T-Piece, and the Bickford, all bypass the carbon dioxide absorbant canister and the one way valves for inspiration and expiration. These valveless systems have less resistance than the circle system. This allows an animals whose muscular strength might be reduced by anesthetic drugs and who is small to make each breath more effective at getting rid of carbon dioxide. The textbooks recommend various size standards : all animals less than 10 kgs should be on it. Does that mean that animal who is 10.9 kgs should be on a circle system? Not necessarily. You can put a larger animal on and increase the oxygen flow rate. How do you know if the non-rebreathing system (NRB) is working? Measure the inspired and expired carbon dioxide with a capnometer or capnography device. If the inspired is zero, you have eliminated enough deadspace and if the end-tidal is 50 or less, you have made the correct choice.
So what is the oxygen flow rate in liters/min? The textbooks vary in suggestion, from 150 ml/kg to 300 ml/kg to 600 ml/kg to prevent the rebreathing of carbon dioxide. The gold-standard way to do this is to use capnography as described above and use the lowest flow that prevents the rebreathing of carbon dioxide. I recommend no less than ½ liter per min per patient and somewhere between 300-600 ml/kg for patients under 10 kg. The higher the flow, the more oxygen and inhalant agent is used.
How should these be integrated with a circle anesthesia system? The fresh gas line for the NRB should connect to the vaporizer outlet or the fresh gas line leading to the circle system but before it enters the system. The waste gases should connect to and F-air canister or to a passive scavenger or to an active scavenger with an adjustable valve so that the gases are not pulled from the patients lungs.
Let us now consider the circle or rebreathing system. It consists of oxygen that flows to a vaporizer which connects to the inspiratory side of the system, usually just after the carbon dioxide absorbant canister. The patient inhales and the one-way valve lifts, gases flow into the tubing and out to the patients. The patient exhales and the expiratory one way valve lifts, the inspiratory valve stays seated to prevent the gases from flowing the wrong direction, and the waste gases enter the carbon dioxide absorbant canister where they react with the granules to remove CO2, add some water to the gases and then enter the inspiratory valve and the reservoir bag. By the way, the proper size of the reservoir bag is 60-90 mls/kg of animal (6 x the tidal volume; tidal volume is 10-15 ml/kg). What should the oxygen flow be? Considering that most general practices are not set up to do low flow or closed system anesthesia, I recommend anywhere from 33-66 ml/kg/min flow of oxygen. We know this meets the metabolic demands of most animals.
What other factors influence respiration? Endotracheal tubes that are properly sized enable respiration. Every tube lessens the airway diameter with reference to the equation for area of πr2. Therefore each size decrease in mm is that number squared decrease in area. Something to keep in mind and have different size tubes available should the patients airway be larger (or smaller) than you expect. It is better for the airway to put in the largest tube possible and use the cuff to form just enough seal to pass the leak test. What other hindrences can be put on the tube? The elbows and bending connectors impair the flow of air, creating more resistence to breathing, so it’s better not to use them but we use them when positioning for the procedure would potentially cause a “kink” or collapse in the tube, obstructing the airway.
Anesthetic drugs depress respiration, by depressing the innate drive to breath in the repiratory centers of the central nervous system and by weakening the muscles of respiration. In addition, we position animals for surgeries or procedures often on their backs, with their limbs extended, and sometimes we cause their visceral to press on vessels and organs that are usually not feeling this weight, press on the diaphragm, and impair the chest and diaphragm expansion. So it is a three-fold attack: 1) reduce the nerve firings that tell the body to breath 2)reduce the strength of themuscle of breathing as a side effect of anesthetic drugs 3)position the animal so that the diaphragm cannot expand and the muscles are in a less than optimal arrangement for breathing. This is why we don’t want to add any more impedances to small patients and so we turn to using NRBs. We want to eliminate the extra work added to breathing of the one way valves and the carbon dioxide absorbant canister.
 West, Pulmonary physiology
 Berne and Levy
 Lumb and Jones
 Lumb and Jones
I confess I love home shows, DIY shows. I am not just jumping on the latest trend- I used to watch This Old House long before they changed hosts. Bob Vila emails me daily. I have noticed a trend I do believe is helpful for managing the active dog and multi-pet household: open concept living. Here are a few takeaways that could promote our favorites species happiness all while justifying watching HGTV. Disclaimer: I am not an expert on behavior, consult a Diplomate of the American College of Veterinary Behavior. I have just lived in a multiple pet households by choice since 1993.
Open concept forces one to reduce clutter. There is no kitchen door to close to hide the dishes or the multiple appliances. Dishes need to be in the dishwasher and the counters need to be wiped. This can help with dogs who guard food, guilty party pictured above. Nothing left to guard except the entire kitchen. That leads us into the next topic.
Lack of doors, lack of points of conflict. Some dogs compete with other dogs for being the first through the door, or prevent access to some household members. Fewer doors, fewer fights. The downside is that now one has to design a few nooks for the less assertive dog to feel secure in without incurring the wrath of the dog who seems to make the rules. Guilty party shown above, laying on his back, saying "who me? I am so sweet!" Instead of crates, I suggest tables to crawl under with no walls around for easy escape. I follow the rule I learned for litter boxes, the number of pets plus 1 is the number of tables for a pet to crawl under. Two dogs need a coffee table, dining table and a desk with no sides. With rugs on pads.
Lack of doors, clear sight lines for praise. The dark ages of punishing pets for training are behind us. Positive reinforcement options abound. When the owner can observe the dog who may choose, even rarely, to inhibit a problematic behavior instant heaps of praise can be given for really small behavioral changes. Praising inhibition can start small changes. It's a type of shaping behavior that is very easy to do while not actually in active training mode. Watch a dog make a small positive change and say "great work you are the BEST dog ever" as though your life depending on convincing the listener that you really mean it. Then motion for them to come over for affection or a treat. So this is really shaping behaviors, not training skills. And having no walls does make the "find me" game pretty boring.
Lack of walls and doors, more space to move freely. Not everyone will love their pets running around and playing in the house, but being able to interact and build the bond of play between dogs has helped my pet family. So, let them play, on the good couch, jump over the wood coffee table, roll around on the rugs. A basket of toys, rotated or replaced, allows the dog choose the object of play. We have no yard, and play with toys is a treat saved for the house. At the fenced-in dog park, we practice our social skills (more later).
Lack of walls forces the footprint of the furniture to count. When you're unable to fill walls with short pieces, the natural good design progression is to build up, and this is where the cats win in the multiple pet household: a place to escape or just enjoy being a skilled athlete. Just secure tall pieces of furniture to the walls. And let the cat jump.
The open concept can a friendly design choice for the multiple pet household by allowing better supervision and better timing of praising, less resources to guard, and more space to bond through supervised play. All while minimizing the clutter and adding peace to a small space. A large home with acres fenced-in and a dog waste management service daily could be wonderful, regardless of design. However, I would miss being part of the small acts of kindness and the nuanced interactions. Having the pets close by and under watch forces one to acknowledge and praise the small good and kind acts, instead of reacting to the loud and unmissable pet disagreements.
To all the DACVB who have helped us, thank you. I still adopt Australian shepherds so I still need your help and I hope you like this article.
One of the most frequent questions I am asked is what is the dose of dexmedetomidine (Dexdomitor®) that one should use and the answer depends on two predictable factors and one unpredictable factor. I could shortcut this entire article by saying about 5 mcg/kg administered intramuscularly or subcutaneously or slowly intravenously,is my starting dose for premedication in dogs, 10 mcg/kg in cats. The predictable factors are what we know: the other medication being administered at about the same time and the procedure that will be competed under the medication's actions.The unpredictable factor is the individual patient's response to the medication. The state of arousal or relaxation may be difficult to interpret in every patient. We also do not know each patient's genetics for medication processing nor receptor types and distribution.
There is a rumor out there that one should throw away the package insert. The dexmedetomidine labeling process probably suffers from being too complex. Sometimes choice is good and sometimes choice is overwhelming. Initially, the label insert had four different dosage classes for dogs; now it is simpler, just two dosages for dogs and one for cats. Within each dosage class, different dosages are suggested for different weight ranges. My dosages in the first paragraph are lower than some of the labeled, proven safe dosages. I defer to FDA approved doses in theory, but I follow my peers and my experience in practice.
If this is making your inner skeptic curious, what is the reasoning for all the dosages? The label has a Preanesthesia ("premedication") dosage, which means the patient becomes mildly sedate, tolerates venous cannulation and experiences a smooth induction without the excitement phase. Often an opioid is administered with the dexmedetomidine. There is a stand-alone higher dose for Sedation/Analgesia, used for quick painful procedures such as radiographing aching joints, laceration repair, or small mass removals.
Dexmedetomidine labeled dosages are based on the body surface area (BSA). This would mean that my dosage of 5 mcg/kg may be equivalent to a 3 mcg/kg in a Great Dane and 9 mcg/kg in a Yorkshire terrier. Usually I add an opioid. I might add ketamine for the fractious patients, or a benzodiazepine (midazolam, for example), or all three, because I am an anesthesiologist and have bought in to the concepts of multimodal analgesia and balanced anesthesia.
What about other unknowable differences? These include variations such as genetics, age, gender and other physiological states that may affect uptake and distribution and ultimately the peak plasma levels of a given medication. The following case examples illustrate the challenges of choosing a safe and effective dosage.
Carson is a 5 yr old MC mixed breed with a lean body and a sweet disposition. He was bitten at the dog park and needed his wound explored and treated. We administered the highest labeled dose of dexmedetomidine IM as a stand-alone drug in an on-label manner. He seemed to respond quickly, his eyes blinked slowly and he relaxed. We waited and he never became deeply sedate. We reversed the dexmedetomidine with an equal volume of atipamezole given IM. Carson is my example of a possible faster metabolizer of the medication. I believe he never reached a peak plasma level consistent with sedation, despite adequate dosing.
Max, a 4-year-old mildly overweight MC Labrador retriever with a sweet disposition was given the labeled Sedation/Analgesia dose. but he did not become sedated enough for radiographs of his stifle even after an hours’ time. The procedure was canceled and Max hopped in the car. No reversal was given. He became unconscious during the drive home and the panic-stricken owner called, unable to rouse Max. He drove him back, and he was administered atipamezole in equal volume to his dose of dexmedetomidine. Max had no ill effects from the experience. The veterinarian was perplexed. How did this happen? I believe Max may have been an example of a slower uptake of dexmedetomidine than expected. I believe he reached his peak plasma level in the car, later than expected.
The last story does not have a happy ending. Fiona, a normal BCS, 7-year-old FS mixed breed who lived outside presented for routine veterinary care. Her previous visit was for her OVH 6 years before. The owner agreed to everything his veterinarian suggested, including blood tests and a dental. Dexmedetomidine and butorphanol were administered at a Preanesthesia dose. The dog was induced with propofol, intubated, and carefully monitored. During the dental cleaning the technician noted that the pulse oximeter did not read but continued the procedure, expecting an improvement. The blood pressure monitor read high blood pressure or failed to read. Her supervising veterinarian was in a room with a client. When the veterinarian returned, the dog was taking extremely deep breaths and he realized Fiona was exhibiting agonal breathing. The reversal atipamezole was administered IM but did not help. Fiona did not survive. We walked through the processes and examined the system errors together as a collaborative process.
It was not definitively the fault of dexmedetomidine but we reported the incident to the manufacturer. The owner accepted the outcome and he paid the bill in full, which made the veterinarian feel worse though he already blamed himself for all the events. While I am not certain dexmedetomidine caused the dog's demise, I do think it contributed to a system-wide error of ignoring anesthesia equipment because of cumulative frustration from using the monitors on patients who are vasoconstricted (more later in another article on monitoring).
What do Carson, Max and Fiona have in common? They all had a response to the medication outside the anticipated range of responses. One can speculate that Carson metabolized the medication faster or had more circulating catecholamines from his situation that counteracted the sedation. Perhaps Max's injection was in adipose tissue instead of an intramuscular injection (veterinarian swore this was not the case) or his uptake and distribution of the medication was slower for other reasons. Perhaps Fiona, who appeared healthy was not. Perhaps she had higher plasma concentrations on the same labeled dose than expected or perhaps the other medications contributed.
Choose the on-label dose, or choose the dose of your peers within the standard or care, and remain aware of the possibility that the patient may not respond in a predictable matter. Develop other systems to identify and respond to that outcome efficiently.
Oxygen supplementation before and after anesthesia is always intended to be helpful and usually is not harmful as long as a short safety check list is implemented. This post will set aside free radical concerns for now. Each practice should make there own checklist, and I have a few suggestions on what the checklist should include.
Is the patient able to exhale carbon dioxide in a manner that allows him/her to not re-breathe the exhaled carbon dioxide? Typical veterinary anesthetic induction masks are supposed to fit with low dead space to avoid rebreathing exhaled gases. This is not a comfortable feeling on a patient who is awake. Try it sometime: have someone place a plastic mask over you and hold you down. Probably you're able to visualize all the unpleasant noxious stimulus without this dramatic role-playing. This leads to number 2.
Is the patient struggling? This means there will likely be a more difficult induction, more medications may be required and the early anesthesia may be more challenging. There will also be more physiological stress and more consumption of oxygen. There is also a subtle undermining of the anesthetic plan. Here's what I think happens: an induction with struggling, leads to catecholamine release which stimulates a cascade that likely probably further compromises in immunity in the long run, but in the short run can lead to a dangerous depth. Initially, with the struggling, more medications or inhalant is added, and then as the patient loses that cardiovascular excitement vital start dropping before inhalant can be reduced.
Is the use of oxygen actually increasing the fraction of inspired oxygen? Sometimes I watch well-intended anesthetists hold a single port of oxygen a few inches away from a patient. This choice is often the result of number 1 in my suggestions. I believe this is doing very little except taking extra effort on the part of the anesthesia team. In the ICU we place patients in oxygen cages, or place nasal cannulas.
Is the use of oxygen supplementation potentially dangerous? Recently, and this is second hand, I was told of a patient for whom the oxygen supplementation was placed inside the ET tube and obstructed the gases and caused barotrauma. If this happened as described, I can believe it. I have removed a few of these lines out of ET tubes placed b well-intervened caregivers with patients in recovery. If preoxygenation is the concern, the patient needs to be sedated to the point of not resenting the mask. That has some problems too. Or the mask can be placed as the animal is being induced, feeling unaware or unable to struggle (another post on that new information), and let the last few breathes before unconsciousness sip the oxygen rich "air" deep into the lungs as a protection against hypoxemia from apnea during intubation.
If supplementing oxygen, it is best to use an anesthesia mask connected to an anesthesia circuit so there is a bag and a valve for excess. If using a separate systems, such as in recovery, be sure it is a bag mask valve, so the oxygen can be provided and the excess can be discarded. Examples are oxygen masks with two valves in the side and the Ambu bag. Both increase the work of breathing but allow safer oxygen supplementation in recovery.
Jennifer Hess is a board-certified anesthesiologist who has a life-long interest in helping high-risk patients survive and thrive after anesthesia.