RESTORE ketamine infusion therapy

RESTORE is a structured course of ketamine infusion therapy for depression and bipolar depression, anxiety, post-traumatic stress disorder, and chronic nerve pain that has not responded to other treatment. We also treat fibromyalgia, complex regional pain syndrome, burnout syndrome, and chronic migraine that has not responded to standard treatment. It was developed at this institute over many years of treating these conditions, and it is deliberately not the way ketamine is usually given.

The pattern most patients encounter is six infusions spread across two to three weeks, with each dose set by body weight, followed by maintenance infusions scheduled by the calendar [2] [4]. That schedule was never arrived at through dose-finding work in psychiatry. Where it did come from is the first thing explained on this page.

RESTORE is built differently on four specific points.

	The schedule most patients encounter [2] [4]	RESTORE
The dose is based on	Your body weight	A target concentration in your blood, modeled from your own measurements
A full first course takes	Six infusions across two to three weeks	Three infusions on three consecutive days, completed in a single visit
The next infusion is decided by	The calendar, at a set interval	Your score on a validated rating scale, repeated over time
During the infusion	Monitoring and staffing vary widely from one practice to another	The standard used for procedural sedation, with a physician present for every minute

The left column describes the treatment schedule that has been carried forward in the literature since the earliest studies of ketamine for depression. It is not a description of any particular clinic.

Each of these differences is explained below, with the evidence behind it.

Two reinforcement infusions follow at two to three months, and then we reassess you formally. Most people who are still doing well need one infusion once or twice a year after that.

Who gives the treatment. Every infusion here is given by Gerald W. Grass, MD, the Institute’s founder and medical director, formerly Assistant Professor of Anesthesiology and Pain Medicine at Yale University School of Medicine and Director of the Yale Pain Medicine Fellowship Program. He first used ketamine clinically in 1989 and has worked with it ever since. He is in the room for every minute of every infusion. More about Dr. Grass

Other physicians come here to learn this method. Since 2016 the Institute has run an intensive training program in which licensed clinicians travel to Sarasota for classroom instruction and supervised clinical training in a working infusion suite. What they are taught is the treatment described on this page. About the training program

What follows is an explanation of why the program is built this way. It is longer than most clinic websites. We think you should understand what is being proposed before you agree to it.

Are you a candidate?

Where the usual ketamine dose came from

Almost every ketamine infusion given for depression in this country follows one recipe. Half a milligram of ketamine for each kilogram of body weight, infused over forty minutes, repeated six times across two or three weeks.

That dose was not chosen because studies showed it was the right amount for depression. It first appears in 1994, in research designed to study what ketamine does to the mind in healthy volunteers [1]. When the first trial of ketamine as an antidepressant was run six years later, it used the dose that was already there [3]. A review of the subject says so plainly. The figure has remained the commonest dose “perhaps by default,” and the forty minute session became the norm because the early studies happened to last forty minutes [2].

Clinics are aware of this. A survey found that most begin at half a milligram per kilogram, but the great majority change the dose during a course of treatment, across a range running to six times the starting figure [4]. The number was meant to be a place to start. It is not always treated as one.

Why two people can get the same dose and not the same result

Ketamine only works while enough of it is in the bloodstream. What counts is not the number of milligrams in the bag. It is how much of the drug is actually in your blood, and how long it stays there. Doctors call that the plasma concentration.

Those two things are not the same. Take two people who both weigh 180 pounds and give them an identical dose. One may reach a blood level in the range where ketamine works and hold it for most of the hour. The other may pass through that range briefly, or never quite reach it. Both had the same infusion. Only one had the treatment.

Bodies handle the drug differently. It does not spread through everyone at the same rate, and the liver does not clear it at the same speed. One study of patients with treatment resistant depression measured this directly. The space the drug spreads into varied by about 47 percent from one person to the next, and the speed of clearance varied by a similar margin [5].

Two liver enzymes do most of the work of breaking ketamine down, called CYP2B6 and CYP3A4 [11,12]. Some people carry gene variants that make those enzymes faster or slower than average. Some medicines speed them up, and others slow them down. Either way, the same infusion can leave two people with very different amounts of drug in the blood.

The part of the body that counts first

When ketamine goes in, it does not reach the whole body at once. It fills the blood first, along with the organs that have the richest blood supply. The brain is one of them. Pharmacologists call this the central compartment. Only afterward does the drug spread out into fat and muscle.

The level in that first compartment is what the brain sees while the infusion is running. And that is the difficulty with dosing by total body weight. As a person gets heavier, the fat and muscle grow considerably. The central compartment does not. Studies of intravenous anesthetics in patients with obesity have found that the central volume changes comparatively little, while the outer volumes grow a great deal [25].

A dose worked out from total body weight therefore delivers too much into the compartment that matters, and delivers it too quickly. That is the point in an infusion when blood pressure climbs and the experience can turn frightening.

The same drug, given two ways. The line that overshoots and then falls away is a dose calculated from body weight. The flat line is a dose calculated to reach and hold a target concentration. The figure illustrates the principle; it is not measured patient data.

We calculate on adjusted body weight instead. It is a standard measure, defined as ideal body weight plus 40 percent of the difference between actual weight and ideal weight [28]. Scaling anesthetic doses this way in patients with obesity is long established practice [26], and ideal or adjusted body weight has been recommended for ketamine in particular [27].

How your dose is worked out, and what happens during the infusion

Before we treat you we build a pharmacokinetic model for you. That is a calculation of how your body will take the drug up, spread it around, and clear it. It draws on your weight and body composition, the other medicines you take, and what we know about how you metabolize drugs. From that we work out the rate and the duration of infusion needed to reach the blood level we are aiming for, and to hold it there.

Then we watch.

From Dr. Grass

I stay in the room for every minute of your infusion.

I am watching two things at the same time. The first is your physiology: your blood pressure, your heart rate, your breathing, the oxygen and carbon dioxide you are moving. The second is how you are actually doing, which I ask you about as we go, because no monitor can tell me that part.

Both of those can change while an infusion is running, and both can be acted on. If your blood pressure rises, I manage it. If the experience is becoming more than you want it to be, I can change the rate. Those decisions get made while it is happening, not reviewed afterward.

Gerald W. Grass, MD

The idea of aiming for a blood level rather than a milligram figure comes from anesthesia, where drugs have been given to a calculated target concentration for decades [21]. Dr. Grass trained in anesthesiology and in pain medicine.

Medicines that change how ketamine works

A patient finishes a course of infusions, reports very little benefit, and goes into the record as a non-responder. Sometimes that is the right conclusion. Sometimes nobody looked at the medicine list.

Benzodiazepines are the best documented. The class includes diazepam, lorazepam, clonazepam, and alprazolam. A systematic review concluded that higher doses can delay the time it takes to respond and can shorten how long the benefit lasts [6]. Individual studies point the same way. Benzodiazepine doses were significantly lower in responders than in non-responders in one series [7]. Concurrent use lengthened the time to response and shortened the time to relapse in another [8]. In a third, a dose above the equivalent of eight milligrams of diazepam predicted a poorer result [9].

Lamotrigine is a more complicated case, and worth understanding if you take it. Lamotrigine reduces the release of glutamate, the signaling chemical whose surge follows ketamine’s action at the NMDA receptor [24]. There is a striking clinical observation that fits. A patient admitted after a lamotrigine overdose was given 250 milligrams of intravenous ketamine, several times an anesthetic dose, and developed no dissociative effect at all [22].

What nobody knows is where the threshold sits. Every human study of the combination has used the same single 300 milligram dose of lamotrigine. No dose ranging study has ever been done, and no figure has been published for the amount at which interference begins [23]. Even at that one dose the studies disagree with each other, and the most careful volunteer study found that lamotrigine reduced ketamine’s dissociative and cognitive effects while increasing its effect on mood [20]. So we treat lamotrigine as something to discuss with your prescriber before treatment, not as a reason to turn you away.

There is also early evidence that blocking opioid receptors interferes with ketamine’s antidepressant action. A small crossover trial found that pretreatment with naltrexone prevented the antidepressant effect while leaving the dissociative effects intact [10]. Twelve patients completed that study and it was stopped early, so the finding is provisional rather than settled. We take it into account anyway, because the cost of being wrong is a wasted course of treatment.

Going through your medicine list is therefore a required step before we accept you. Where something you take may interfere, we talk to your prescriber before your first infusion rather than after your last.

The RESTORE Rescue Program

• A complete first course in three days. Three infusions on three days in a row.
• Dosing calculated for your body, not your body weight.
• A physician in the room for the whole of every infusion. One patient at a time.
• Measured follow-up, so a further infusion happens when the scores say it is due.
• 245 days. The average interval before a maintenance infusion was needed in our own review.
• Your records read before we accept you, and an honest answer about whether this is for you.

How ketamine works

Ketamine blocks a receptor in the brain called the NMDA receptor. That produces a short lived rise in glutamate, the brain’s main excitatory signaling chemical, and sets off a chain of events linked to the growth of new connections between nerve cells [13,14]. Ketamine also acts at a large number of other targets, which is one reason its effects are hard to sum up in a sentence [15,16].

The understanding of depression that best fits these findings is not a simple chemical shortage. It is a problem in the communication between regions of the brain. Ketamine appears to act on that communication, and that offers one explanation for its unusual timing.

Conventional antidepressants generally take several weeks to work. Ketamine has been shown to produce measurable improvement within hours. In a controlled trial in treatment resistant depression, seventeen of eighteen patients improved significantly within two hours of a single infusion, and 71 percent met the criteria for response at twenty four hours [17]. A later trial at two sites confirmed the finding [18].

Safety and monitoring

Ketamine is an anesthetic. At the doses used to treat depression and pain it changes consciousness, it moves blood pressure and heart rate, and it can affect the reflexes that protect your airway.

Why we watch this closely

None of this is here because ketamine is dangerous in the way people sometimes fear. It is here because ketamine is an anesthetic, and anesthesia spent forty years building a monitoring standard that turned a hazardous specialty into one of the safest things in medicine. That progress did not come mainly from better drugs. It came from watching continuously, so that a change is noticed while it is still small and easily corrected.

That is the standard we use here. It means the answer to the question “how are you doing right now” is never an estimate. Your oxygen, your breathing, your heart rhythm, and your blood pressure are measured second by second, and a physician trained in airway management is with you, reading them as they happen.

The practical effect is a calmer treatment, not a more worrying one. Most infusions pass without incident. Careful monitoring is a large part of the reason why, because small changes get corrected early, while they are still small, and before they become anything you would notice.

Ketamine’s reputation for being well tolerated is deserved. It is also the reason it is sometimes given with lighter monitoring than an anesthetic warrants, and published surveys of community ketamine practice report wide variation in how these treatments are monitored [4]. We treat every infusion as an anesthetic administration, every time.

We monitor at the standard used for procedural sedation. Every infusion, for every patient:

Continuous pulse oximetry, with audible alarms.
Capnography. It measures the carbon dioxide you breathe out, which picks up a breathing problem before your oxygen level starts to fall.
Cardiac monitoring and automatic blood pressure readings.
A formal airway assessment before every infusion, recorded as a required step rather than left to the clinician’s discretion.
Emergency airway equipment and medicines immediately at hand, together with the training to rescue a patient from one level of sedation deeper than the level intended.
Depth of sedation scored on a validated scale rather than estimated by eye, with a formal check before treatment starts.
A structured discharge routine: recovery scoring, repeated blood pressure readings, a psychiatric safety screen, a minimum observation period, and written instructions to take home.

Emergency equipment is a precaution, not a prediction. It is kept ready for the same reason an anesthesiologist keeps it ready in an operating room where nothing is expected to go wrong, and in the great majority of infusions it is never needed.

We treat one patient at a time. There are never several infusions running at once, no clinician moving between rooms, and no point in your treatment when the physician caring for you is attending to someone else. The dose was worked out for you, and the adjustments made while it runs are made for you, in response to what your body and your mind are doing that day. From the moment your infusion begins until you are ready to go home, our attention is yours.

Safety, risks and limits

Before we accept you

Whether you are a candidate is a clinical decision, not a booking. We read your treatment history, your current medicines, and the relevant laboratory work before we take you on.

Some people we turn down. It may be a medical reason that rules ketamine out. It may be that ketamine is unlikely to help the particular problem you have. It may be that something else needs attention first. We would rather tell you that on the phone than after you have paid for a flight.

Where something can be put right before treatment starts, we deal with it first. That might be a change of medicine, agreed with the doctor who prescribes it. It might be correcting a metabolic problem. Where genetic testing of the enzymes that break down your medicines would change the plan, we may suggest a commercially available panel.

Are you a candidate?

The course of treatment

The first course is three infusions on three days in a row, finished in a single visit. Two reinforcement infusions follow at two to three months, and then we reassess you. Most people who are still doing well need one infusion once or twice a year after that.

You are scored on a validated rating scale before treatment and at intervals afterward. That way, whether the treatment is working is a question with an answer. It also means a further infusion happens when the score says it is due, rather than when a month has gone by.

What we found when we looked at our own patients

We reviewed sixty months of our own patients treated for treatment resistant depression. Eighty seven people, scored on the Beck Depression Inventory-II.

Of the eighty seven who started, seventy eight finished the full protocol. Counting everyone who started, which is the harder way to count, 79 percent responded and 51 percent reached remission. Among those who completed the full course, 88.4 percent responded and 56.3 percent reached remission. The average time before a maintenance infusion was needed was 245 days.

This was a look back at one practice. There was no control group and no blinding, and it has not been peer reviewed. We say so because a number offered without its limits is not worth much. These are our own patients, looked at in retrospect. They are not a prediction of what will happen to you.

SEE WHETHER YOU ARE A CANDIDATE

Or call 800-850-6979 and speak to us directly. We will tell you honestly whether this is likely to help you.

Our results, and how to read them

What ketamine cannot do

Ketamine is approved by the Food and Drug Administration as an anesthetic. It is not approved for depression, anxiety, post-traumatic stress disorder, or chronic pain, and using it for those conditions is off-label [19]. Off-label prescribing is lawful and ordinary in medicine. You are still entitled to know that this is what is being offered.

Ketamine is not a cure. For most people who respond it is a treatment that has to be maintained. Some people get no benefit at all, and we cannot tell in advance who they will be. There are real risks, there are real reasons not to give it, and there are people we decline to treat.

If you are having thoughts of harming yourself, call or text 988 to reach the Suicide and Crisis Lifeline, or go to your nearest emergency department. Ketamine therapy is scheduled care. It is not a substitute for emergency treatment.

How this program was developed

RESTORE was not taken from a protocol found in the literature and put into practice. It was built here, over a long stretch of clinical work with ketamine that began before anyone was using the drug for depression at all.

1989. Dr. Grass first used ketamine clinically during a neurosurgical residency rotation, and went on using it through his training in emergency medicine and in anesthesiology. At that time ketamine was an anesthetic and nothing more. Its effect on depression had not yet been described.

2000. The first controlled trial of ketamine in depression was published from Yale [3]. Dr. Grass later held a faculty appointment in anesthesiology and pain medicine at that institution and directed its Pain Medicine Fellowship Program.

2005. Holding a joint appointment at the Yale Department of Anesthesiology and Pain Medicine and at the Veterans Administration Department of Anesthesiology, where he served as Chief of Pain Management, he began treating veterans with ketamine.

Building the dosing method. The conventional dose is a number multiplied by your weight. Working from the published pharmacokinetics of ketamine and from the way the drug actually distributes in the body, the Institute moved to dosing against a target concentration in the central compartment instead, and to calculating that dose on adjusted body weight rather than total body weight [5] [11] [26] [27] [28]. This is the single largest difference between RESTORE and the schedule most patients encounter, and it is what makes a shorter, more concentrated course workable.

2016. Dr. Grass founded the Institute’s intensive training program, so that the method could be taught rather than kept. Licensed clinicians travel here for classroom instruction and supervised clinical training in a working infusion suite.

Sixty months of measurement. Outcomes for eighty seven patients treated for treatment resistant depression were scored on a validated rating scale and reviewed as a group, with the response rates, the remission rates, and the average interval before a further infusion was needed all set out on this page, together with the limits of that kind of review.

The three day course is the end of that process, not the beginning of it. Every part of it, the dose, the interval, the monitoring, and the point at which you are reassessed, was arrived at by treating patients and measuring what happened.

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About the Ketamine Research Institute

We do one thing. The Ketamine Research Institute in Sarasota, Florida provides ketamine based infusion therapy and trains clinicians to deliver it. We do not offer other services, and we do not plan to.

Gerald W. Grass, MD, Founder and Medical Director

Before founding the Ketamine Research Institute, Dr. Grass was Assistant Professor of Anesthesiology and Pain Medicine at Yale University School of Medicine and Director of the Yale Pain Medicine Fellowship Program. He has held academic appointments in anesthesiology and pain medicine at Mount Sinai/NYU Medical Center and at the State University of New York at Stony Brook, and in neurological surgery and general surgery at the State University of New York at Buffalo.

Yale is where the first controlled studies of ketamine for depression were carried out. Dr. Grass taught and practiced there. His view of the standard protocol, that the dose used in those early studies was never meant to be a finished treatment plan, is the assessment of a physician trained at the institution where the work began.

Thirty-seven years of clinical experience with ketamine

Dr. Grass first used ketamine clinically in 1989, during his neurosurgical residency rotation, and went on using it throughout his training in emergency medicine and anesthesiology.

In 2005, holding a joint appointment at the Yale Department of Anesthesiology and Pain Medicine and at the VA Department of Anesthesiology and Pain Medicine, where he served as Chief of Pain Management, he began treating veterans. They were soldiers returning from Iraq and Afghanistan with complex chronic pain, depression, and post-traumatic stress. That work is where RESTORE began. In 2006 he started treating private patients.

He has given thousands of ketamine based infusions and has been personally present for the whole of every one, monitoring and adjusting each infusion himself. The RESTORE protocols came out of that experience. They were not adapted from a published paper. They were built from ketamine concentrations measured in plasma during infusions he conducted himself.

Clinical background

Dr. Grass is broadly trained across anesthesiology, neurosurgery, pain medicine, and emergency medicine, with clinical experience in hospital practice, private practice, academic medicine, research, and clinical trials. That range shows in how the RESTORE program is built. Aiming at a target blood concentration is a technique from anesthesiology. The concentration targets used for nerve pain come from pain medicine. The airway assessment and sedation monitoring that make it appropriate to give an anesthetic outside an operating room come from both.

Research and teaching

Dr. Grass is a published author and lecturer whose work includes peer reviewed articles, abstracts, book chapters, and educational presentations. He has presented his research at regional and national conferences and meetings, and to government agencies including the Veterans Administration and the Department of Defense. In 2016 he founded the Institute’s intensive training program for clinicians, which teaches the precision medicine and targeted infusion methods used here through classroom instruction and supervised clinical training in a working infusion suite.

Working with the physicians who already care for you

Ketamine therapy is one part of your care, not a replacement for it. You keep your psychiatrist, your primary care physician, and any specialist treating your pain. We are not asking you to choose between us and them.

We work with them directly. Before we treat you, we go over your history and every medicine you take with the clinician who prescribes it, because several common medicines change the way ketamine behaves in the body, and that has to be settled before an infusion rather than discovered during one [6] [22]. Through your course of treatment and afterward, your own physicians get what they need from us to make their decisions well: what you were given, how you responded, and what we recommend next. We stay available to them for as long as you are our patient.

This coordination is part of the treatment, not a formality. Ketamine can change how a patient is doing within days rather than months, and the decisions that follow, about your other medicines, your therapy, and how closely you are watched, are made better by physicians who are working from the same information we are.

We do treat patients with active suicidal thinking, but only on the recommendation of their psychiatrist, and only with that psychiatrist continuing to co-manage their care.

Learn more about Dr. Grass For referring clinicians

References

Every clinical statement on this page is referenced below. Where a number appears in the text, it points to the source listed here.

1. Krystal JH, Karper LP, Seibyl JP, et al. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Arch Gen Psychiatry. 1994;51(3):199-214. PMID 8122957.

2. Andrade C. Ketamine for depression, 4: In what dose, at what rate, by what route, for how long, and at what frequency? J Clin Psychiatry. 2017;78(7):e852-e857. PMID 28749092.

3. Berman RM, Cappiello A, Anand A, et al. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry. 2000;47(4):351-354. PMID 10686270.

4. Wilkinson ST, et al. An Update on Community Ketamine Practices. Am J Psychiatry. 2022. PMID 35491568.

5. Abuhelwa AY, Somogyi AA, Loo CK, et al. Population Pharmacokinetics and Pharmacodynamics of the Therapeutic and Adverse Effects of Ketamine in Patients With Treatment-Refractory Depression. Clin Pharmacol Ther. 2022;112(3):720-729. PMID 35560226.

6. Veraart JKE, Smith-Apeldoorn SY, Bakker IM, et al. Pharmacodynamic Interactions Between Ketamine and Psychiatric Medications Used in the Treatment of Depression: A Systematic Review. Int J Neuropsychopharmacol. 2021;24(10):808-831. PMID 34170315.

7. Frye MA, Blier P, Tye SJ. Concomitant benzodiazepine use attenuates ketamine response. J Clin Psychopharmacol. 2015. PMID 25928701.

8. Albott CS, Shiroma PR, Cullen KR, et al. The Antidepressant Effect of Repeat Dose Intravenous Ketamine Is Delayed by Concurrent Benzodiazepine Use. J Clin Psychiatry. 2017;78(3):e308-e309. PMID 28394513.

9. Andrashko V, Novak T, Brunovsky M, et al. The Antidepressant Effect of Ketamine Is Dampened by Concomitant Benzodiazepine Medication. Front Psychiatry. 2020;11:844. PMID 33005153.

10. Williams NR, Heifets BD, Blasey C, et al. Attenuation of Antidepressant Effects of Ketamine by Opioid Receptor Antagonism. Am J Psychiatry. 2018;175(12):1205-1215. PMID 30153752.

11. Peltoniemi MA, Hagelberg NM, Olkkola KT, Saari TI. Ketamine: A Review of Clinical Pharmacokinetics and Pharmacodynamics in Anesthesia and Pain Therapy. Clin Pharmacokinet. 2016;55(9):1059-1077. PMID 27028535.

12. Hijazi Y, Boulieu R. Contribution of CYP3A4, CYP2B6, and CYP2C9 isoforms to N-demethylation of ketamine in human liver microsomes. Drug Metab Dispos. 2002;30(7):853-858. PMID 12065445.

13. Li N, Lee B, Liu RJ, et al. mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists. Science. 2010;329(5994):959-964. PMID 20724638.

14. Krystal JH, Kavalali ET, Monteggia LM. Ketamine and rapid antidepressant action: new treatments and novel synaptic signaling mechanisms. Neuropsychopharmacology. 2024;49(1):41-50.

15. Zanos P, Gould TD. Mechanisms of ketamine action as an antidepressant. Mol Psychiatry. 2018;23(4):801-811. PMID 29532791.

16. Zanos P, Moaddel R, Morris PJ, et al. Ketamine and Ketamine Metabolite Pharmacology: Insights into Therapeutic Mechanisms. Pharmacol Rev. 2018;70(3):621-660. PMID 29945898.

17. Zarate CA Jr, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006;63(8):856-864. PMID 16894061.

18. Murrough JW, et al. Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial. PMID 23982301.

19. KETALAR (ketamine hydrochloride) injection, prescribing information. NDA 016812, initial US approval 1970. US Food and Drug Administration.

20. Anand A, Charney DS, Oren DA, et al. Attenuation of the neuropsychiatric effects of ketamine with lamotrigine. Arch Gen Psychiatry. 2000;57(3):270-276. PMID 10711913.

21. Target-controlled infusion, past, present, and future. J Anaesthesiol Clin Pharmacol. 2024. PMID 39391641.

22. Kornhall D, Nielsen EW. Failure of ketamine anesthesia in a patient with lamotrigine overdose. Case Rep Crit Care. 2014;2014:916360. PMID 25114807.

23. Wilkowska A, Wiglusz MS, Jakuszkowiak-Wojten K, Cubala WJ. Ketamine and Lamotrigine Combination in Psychopharmacology: Systematic Review. Cells. 2022;11(4):645. PMID 35203296.

24. Cunningham MO, Jones RSG. The anticonvulsant lamotrigine decreases spontaneous glutamate release but increases spontaneous GABA release in the rat entorhinal cortex in vitro. Neuropharmacology. 2000;39(11):2139-2146. PMID 10963757.

25. Kim TK. Obesity and anesthetic pharmacology: simulation of target-controlled infusion models of propofol and remifentanil. Korean J Anesthesiol. 2021;74(6):478-487. PMID 34407372.

26. Ingrande J, Lemmens HJM. Dose adjustment of anaesthetics in the morbidly obese. Br J Anaesth. 2010;105(Suppl 1):i16-i23. PMID 21148651.

27. Erstad BL, Barletta JF. Drug dosing in the critically ill obese patient. Crit Care. 2020;24:315. DOI 10.1186/s13054-020-03040-z.

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800 850 6979

Ketamine infusion therapy, dosed to a measured target rather than to your body weight

A complete first course of treatment in three days
A physician in the room for every minute of every infusion
Call Us Today: 800-850-6979

RESTORE ketamine infusion therapy

Where the usual ketamine dose came from

Why two people can get the same dose and not the same result

The part of the body that counts first

Call 800-850-6979 and we will tell you honestly whether you are a candidate.