{"id":5366,"date":"2011-07-14T20:25:52","date_gmt":"2011-07-14T20:25:52","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5366.htm\/"},"modified":"2015-02-07T19:25:04","modified_gmt":"2015-02-08T00:25:04","slug":"procedural-sedation","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/resuscitation\/sedation\/procedural-sedation.htm\/","title":{"rendered":"Procedural Sedation"},"content":{"rendered":"<h4>Larson&#8217;s Point for Laryngospasm<\/h4>\n<p>(Anesthesiology: November 1998 &#8211; Volume 89 &#8211; Issue 5 &#8211; p 1293\u20131294)<\/p>\n<h4><\/h4>\n<h4><a href=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/the-magic-point.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-thumbnail wp-image-8716\" title=\"the magic point\" src=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/the-magic-point-150x150.jpg\" alt=\"\" width=\"150\" height=\"150\" \/><\/a><a href=\"https:\/\/crashingpatient.com\/resuscitation\/procedural-sedation.htm\/attachment\/larsons-point-2\/\" rel=\"attachment wp-att-8783\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-thumbnail wp-image-8783\" title=\"larson's point\" src=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/larsons-point-150x150.jpg\" alt=\"\" width=\"150\" height=\"150\" \/><\/a><\/h4>\n<h4><a href=\"\/wp-content\/pdf\/planes%20of%20anesthesia.pdf\">Planes of Anesthesia<\/a><\/h4>\n<p>Annals recs for credentialing, privileges, and practice (Ann Emerg Med 2011;58(4):365)<\/p>\n<p>Who owns deep sedation editiorial (by Steve Green Ann Emerg Med 2011)<\/p>\n<h3><span class=\"ez-toc-section\" id=\"ASA_Classification\"><\/span>ASA Classification<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<ul>\n<li><strong>Class 1<\/strong> Healthy patient, no medical problems<\/li>\n<li><strong>Class 2 <\/strong> Mild systemic disease<\/li>\n<li><strong>Class 3<\/strong> Severe systemic disease, but not incapaitating<\/li>\n<li><strong>Class 4<\/strong> Severe systemic disease that is a constant threat to life<\/li>\n<li><strong>Class 5 <\/strong> Moribund, not expected to live 24 hours irrespective of operation<\/li>\n<li>An <strong>e <\/strong>is added to the status number to designate an emergency operation. An organ donor is usually designated as Class 6<\/li>\n<\/ul>\n<h3><span class=\"ez-toc-section\" id=\"Levels_of_Sedation\"><\/span>Levels of Sedation<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p><a href=\"\/wp-content\/images\/part1\/sedation%20levels.jpg\"> <img decoding=\"async\" src=\"\/wp-content\/images\/part1\/sedation%20levels_small.jpg\" alt=\"\" \/><\/a><\/p>\n<p>&nbsp;<\/p>\n<p><a href=\"\/wp-content\/images\/part1\/sedation%20recovery%20graph.jpeg\"> <img decoding=\"async\" src=\"\/wp-content\/images\/part1\/sedation%20recovery%20graph_small.jpeg\" alt=\"\" \/><\/a><\/p>\n<p>Deep sedation by EPs is safe (W J EM 2011;12(4):399)<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Fasting\"><\/span>Fasting<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p><a href=\"\/wp-content\/images\/part1\/fasting%20in%20sedation.jpg\"> <img decoding=\"async\" src=\"\/wp-content\/images\/part1\/fasting%20in%20sedation_small.jpg\" alt=\"\" \/><\/a><\/p>\n<p>review states only one case of aspiration in all of the literature (Emerg Med J 2010;27:254e261)<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Peds\"><\/span>Peds<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Fasting not necessary (Annals EM 42:5, November 2003)<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Hemodynamic_Characteristics\"><\/span>Hemodynamic Characteristics<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>In healthy patients, midazolam had no effects<\/p>\n<p>dex &gt; propofol in BP reductions<\/p>\n<p>Dex also reduced HR<\/p>\n<p>(J Clin Anesth 2011;23:218)<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Dexmedetomidine\"><\/span>Dexmedetomidine<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Precedex<\/p>\n<p>&nbsp;<\/p>\n<p>First case report (Eur J Emerg Med 2010;17(1):60)<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Ketamine\"><\/span>Ketamine<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>New Annals Guidelines by Green &amp; Krauss (Ann Emerg Med 2011; )<\/p>\n<p>best article (Anaesthesia 2007;62(Sup 1):48-53<\/p>\n<p><a href=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/12\/ketamine-advances-article1.pdf\">Ketamine Review from Pharm Journal<\/a><\/p>\n<p>Green&#8217;s study of overdose show a remarkable degree of safety (ANNALS OF EMERGENCY MEDICINE 1999;34(4):492)<\/p>\n<h4><a href=\"http:\/\/freeemergencytalks.net\/2012\/07\/baruch-krauss-usa-2012-06-28-d2t2-1030-ketamine-in-the-emergency-department\/\">Krauss Free Emergency Lecture<\/a><\/h4>\n<p>neck\/face rash common, not IgE mediated<\/p>\n<p>1 pass drugs (propofol, etomidate, ketamine, sux, brevitol, thiopental, adenosine)<\/p>\n<p>If pt has diplopia, ask them to close 1 eye<\/p>\n<p><strong>How Krauss gives ketamine to kids<\/strong><\/p>\n<p>0.5 mg\/kg q 5 minutes x 3, maybe 4 doses for longer procedures<\/p>\n<p>when the pt is &gt;50 kg he doses lower. He gives 25 mg aliquots until the pt is where he wants.<\/p>\n<p>IM Dosing: sub-disassoc 2mg\/kg; disassoc 4-5 mg\/kg<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Is lamotrigine the antidote to the hallucinations (<a href=\"http:\/\/www.scancrit.com\/2012\/05\/28\/lamotrigine-ketamine-match\/\" target=\"_blank\">from ScanCrit<\/a>\u00a0 <a href=\"https:\/\/crashingpatient.com\/resuscitation\/procedural-sedation.htm\/attachment\/from-the-scancrit-guys\/\" rel=\"attachment wp-att-8780\">pdf<\/a>)<\/p>\n<p>For perioperative pain (Anesth 2005;102:211) 0.5 mg\/kg bolus and then same per hour<\/p>\n<p>Ketamine Activates Breathing and Abolishes the Coupling between Loss of Consciousness and Upper<br \/>\nAirway Dilator Muscle Dysfunction in rats (ANESTHESIOLOGY 2012; 116:6\u20138.)<\/p>\n<p>Preserves Laryngeal Reflexes (Anesthesiology 1973; 38:128 \u201333)<br \/>\nsuggestion actually works to prevent ketamine bad trips (Anesthesia &amp; Analgesia 2011;112(5):1082)<\/p>\n<p>Case of laryngospasm (no actual spasm visualized) from prehospital ketamine (Burnett AM, PREHOSPITAL EMERGENCY CARE 2012;Early Online:1\u20133)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Review of pharm (<strong><em>Current Drug Targets, <\/em>2005<em>, 6, <\/em>789-794)<\/strong><\/p>\n<p>alpha of 45 minutes<\/p>\n<p>terminated by redistrib from cns and hepatic p450<\/p>\n<p>increases CBF, so may increase CBV<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>A low dose infusion gives analgesia<\/p>\n<p>Injections give analgesia and anxiolysis<\/p>\n<p>High Doses give amnesia and disassociation<\/p>\n<p>Cautions<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Central adrenergic release, premedication with depressants (benzos) or fentanyl will probably blunt this response.<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 MAP increased ~25 mmHg<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Probably has neuroprotective effect by NDMA antagonism, so probably will be allowed to be used in stroke and head injury in the future.<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 True laryngospasm is exceedingly rare, probably just tongue obstruction.\u00a0 Inevitably resolves with airway positioning.<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 The intraocular pressure increase has only been reported in animals<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Avoid in hyperthyroid states due to catecholamine release<\/p>\n<p>Premedication<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Glycopyrolate .01 mg\/kg, not to exceed .2 mg or atropine .01 mg\/kg not to exceed .5 mg (can go in same syringe as ketamine, though usually better to give 10-20 minutes beforehand)<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Benzos totally unnecessary in kids, probably not to be used for routine in adults as will prolong recovery times.\u00a0 Use when\/if emergence reaction.\u00a0 Recovery period must be quiet, take off BP cuff, keep in calm environment.<\/p>\n<p>Dosing<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 IM 4 mg\/kg (4-10) or for just analgesia 1 mg\/kg<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Booster Doses 2-5 mg\/kg q 10 minutes<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Use 100 mg\/cc formulation<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Infusion is probably best route for adults<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Mix up bag 1 mg\/cc<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 .15 mg\/kg\/min until sedation then drop down to half that dose<\/p>\n<p>\u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Injection 1 mg\/kg (ETOH 3 mg\/kg)<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 .5-1 mg\/kg booster doses q 10 minutes<\/p>\n<p>o\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Give slowly to prevent apnea from blunted hypercapnia reflexes<\/p>\n<p>&nbsp;<\/p>\n<p>Ketamine 1-2 mg\/kg IV, give atropine beforehand (can go in same syringe), .5-1 mg\/kg\/hr infusion<\/p>\n<h4>Head Injury<\/h4>\n<p>Safety of sedation with ketamine and versed in severe head injury patients: comparison with sufentanil. No increases in ICP, comparable to the fentanyl derivative 25 patients (Crit Care Med. 2003 Mar;31(3):711-7)<\/p>\n<p>and (Crit Care Med 2005;33(5):1109)<\/p>\n<p>and (Ann Emerg Med 2015;65:43)<\/p>\n<p>(Emergency Medicine Journal 2007;24:794-795) Cerebral blood flow (CBF) is critically dependant on cerebral perfusion pressure (CPP) and oxygenation in acute head injuries. Optimal CPP is achieved by maintaining a normal mean arterial pressure (MAP) and limiting iatrogenic increases in intracranial pressure (ICP).1 Brain tissue has high oxygen consumption and no reserves; hypoxia therefore has rapid and profound effects. Early tracheal intubation and ventilation can help prevent hypoxia and aspiration. Hypoxia and hypotension in traumatic brain injury are associated with a 75% mortality rate.2 End tidal carbon dioxide should be maintained around 5 kPa, as hypercapnia causes cerebral vasodilation and increased ICP.3 Ketamine, a potent analgesic, can be used for dissociative anaesthesia in higher doses (2 mg\/kg), or sedation in lower doses. It has a rapid onset and relatively short duration of action (5\u009610 min). Unlike other commonly used induction agents, ketamine does not suppress respiratory activity or airway reflexes; it also has a positive effect on gut motility, and vomiting after administration is uncommon. These properties make it the ideal agent when profound analgesia and sedation are required without a definitive airway in place.3 Ketamine causes increased catecholamine release and decreased norepinephrine (noradrenaline) re-uptake which results in increased heart rate, arterial pressure, and MAP. This makes it a useful analgesic for trauma patients who may already be haemodynamically compromised. A single episode of hypotension is associated with a worse outcome.2 Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist. Head injury increases concentrations of glutamate, which induces neuronal apoptosis. Ketamine blocks the actions of glutamate on the NMDA receptor, which may protect against cellular neurotoxicity, but this has yet to be demonstrated in human studies.1 3 4 Despite these benefits, the use of ketamine in patients with head injuries remains controversial. Early studies suggested that the use of ketamine may have resulted in a transient increase in ICP in a small number of patients.3 CPP was compromised only in the patients with pre-existing intracranial hypertension and obstruction to the flow of cerebral spinal fluid. This has, however, led to the persistent belief that ketamine is contraindicated in patients with traumatic head injuries. Studies done subsequently have shown, however, that the effects of ketamine on cerebral haemodynamics and ICP are in fact variable and depend on both the presence of additional anaesthetic agents and PaCO2 values.5 This patient was sedated with midazolam 10 mg iv, which prevents the emergence phenomenon, and ventilation was controlled artificially en route to hospital. When ketamine is used in the presence of controlled ventilation, in conjunction with anaesthetics which reduce cerebral metabolism such as {gamma}-aminobutyric acid (GABA) receptor agonists, ICP is not increased.1 4 1. Alban\u00e8se J, Arnaud S, Rey M, et al. Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology 1997; 87: 1328\u009634.[CrossRef][Medline] 2. Anon. Prehospital Trauma Life Support Committee of the National Association of Emergency Medical Technicians in Cooperation with The Committee on Trauma of The American College of Surgeons. PHTLS , 6th ed, 2007: 194\u0096221. 3. Sehdev RS, Symmons DAD, Kindl K. Ketamine for rapid sequence induction in patients with head injury in the emergency department. Emerg Med Australas 2006; 18: 37\u009644.[CrossRef][Medline] 4. Himmelseher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005; 101: 524\u009634.[Abstract\/Free Full Text] 5. Mayberg TS, Lam AM, Matta BF et al. Ketamine does not increase cerebral blood flow velocity or intracranial pressure during isoflurane\/nitrous oxide anaesthesia in patients undergoing craniotomy. Anesth Analg 1995; 81: 84\u00969.[Abstract]<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>J Neurosurg Pediatr. 2009 Jul;4(1):40-6.LinksEffectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN.Paediatric Critical Care and.Object Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine&#8217;s use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase-but may rather decrease-ICP. Methods The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (&gt; 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1-1.5 mg\/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration. Results The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 +\/- 8.4 to 18.0 +\/- 8.5 mm Hg) (p &lt; 0.001) and CPP increased from 54.4 +\/- 11.7 to 58.3 +\/- 13.4 mm Hg (p &lt; 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by &gt; 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 +\/- 9.1 to 17.5 +\/- 9.1 mm Hg) (p &lt; 0.0001) following ketamine administration. Conclusions In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Clinical guidelines in Peds (Ann Emerg Med. 2004;44:460-471)<\/p>\n<p>&nbsp;<\/p>\n<p>Probably no difference with or without antisalagogue (Acad Emerg Med. 2003;10:482-483.)<\/p>\n<p>&nbsp;<\/p>\n<p>Case series of use in mentally disabled adults (Acad Emerg Med 1999 6(1):86)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Purpose To define the guidelines for patient selection, administration, monitoring, and recovery for ED dissociative sedation. Definition of Dissociative Sedation d A trancelike cataleptic state induced by the dissociative agent ketamine, characterized by profound analgesia and amnesia, with retention of protective airway reflexes, spontaneous respirations, and cardiopulmonary stability. Characteristics of the Ketamine \u0091\u0091Dissociative State\u0092\u0092 d Dissociation: After administration of ketamine, the patient passes into a fugue state or trance. The eyes may remain open, but the patient does not respond. d Catalepsy: Normal or slightly enhanced muscle tone is maintained. On occasion, the patient may move or be moved into a position that is selfmaintaining. Occasional muscular clonus may be noted. d Analgesia: Analgesia is typically substantial or complete. d Amnesia: Total amnesia is typical. d Maintenance of airway reflexes: Upper airway reflexes remain intact and may be slightly exaggerated. Intubation is unnecessary, but occasional repositioning of the head may be necessary for optimal airway patency. Suctioning of hypersalivation may occasionally be necessary. d Cardiovascular stability: Blood pressure and pulse rate are not decreased and typically are mildly increased. d Nystagmus: Nystagmus is typical. Indications d Short, painful procedures, especially those requiring immobilization (eg, facial laceration, burn debridement, fracture reduction, abscess incision and drainage, central line placement, tube thoracostomy). d Examinations judged likely to produce excessive emotional disturbance (eg, pediatric sexual assault examination). Contraindications: Absolute (Risks Essentially Always Outweigh Benefits) d Age younger than 3 months (higher risk of airway complications) d Known or suspected psychosis, even if currently stable or controlled with medications (can exacerbate condition) Contraindications: Relative (Risks May Outweigh Benefits) d Aged 3 to 12 months (higher risk of airway complications) d Procedures involving stimulation of the posterior pharynx (higher risk of laryngospasm) d History of airway instability, tracheal surgery, or tracheal stenosis (presumed higher risk of airway complications) d Active pulmonary infection or disease, including upper respiratory infection or asthma (higher risk of laryngospasm) d Known or suspected cardiovascular disease, including angina, heart failure, or hypertension (exacerbation due to sympathomimetic properties of ketamine). Avoid ketamine in patients who are already hypertensive and in older adults with risk factors for coronary artery disease. d Head injury associated with loss of consciousness, altered mental status, or emesis (elevated intracranial pressure with ketamine) d Central nervous system masses, abnormalities, or hydrocephalus (elevated intracranial pressure with ketamine) d Glaucoma or acute globe injury (elevated intraocular pressure with ketamine) d Porphyria, thyroid disorder, or thyroid medication (enhanced sympathomimetic effect) Personnel d Dissociative sedation is a 2-person procedure, 1 (eg, nurse) to monitor the patient and 1 (eg, physician) to perform the procedure. Both must be knowledgeable about the unique characteristics of ketamine. d Avoid dissociative sedation when personnel are not experienced with ketamine or may not have time to perform such sedation properly. Presedation d Perform a standard presedation assessment d Educate accompanying family about the unique characteristics of the dissociative state, especially if they will be present during the procedure or recovery.<\/p>\n<p>&nbsp;<\/p>\n<p><strong>Atropine and Glycopyrrolate <\/strong> glycopyrrolate 0.2 mg both pregnancy class B<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Emergence_Reaction\"><\/span>Emergence Reaction<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Hatzskorzian R, Li Pi Shan W, C\u00f4t\u00e9 AV, Schricker T, Backman SB. The management of severe emergence agitation using droperidol. Anaesthesia 2006; 61: 1112\u00965. 2 Malviya S, Voepel-Lewis T, Ramamurthi R, Burke C, Tait AR. Clonidine for the prevention of emergence agitation in young children: efficacy and recovery profile. Pediatric Anesthesia 2006; 16: 554\u00969.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Study results were published in the <strong>August issue of the Archives of General Psychiatry.<\/strong> &#8220;The public health implications of being able to treat major depression this quickly would be enormous,&#8221; said NIH Director Elias A. Zerhouni, M.D. &#8220;These new findings demonstrate the importance of developing new classes of antidepressants that are not simply variations of existing medications.&#8221; For this study 18 treatment-resistant, depressed patients were randomly assigned to receive either a single intravenous dose of ketamine or a placebo (inactive compound). Depression improved within one day in 71 percent of all those who received ketamine, and 29 percent of these patients became nearly symptom-free within one day. Thirty-five percent of patients who received ketamine still showed benefits seven days later. Participants receiving a placebo infusion showed no improvement. One week later, participants were given the opposite treatment, unless the beneficial effects of the first treatment were still evident. This &#8220;crossover&#8221; study design strengthens the validity of the results.<\/p>\n<p>&nbsp;<\/p>\n<p><a href=\"#bbib56\">56<\/a> C.R. Chudnofsky, J.E. Weber and P.J. Stoyanoff <em>et al.<\/em>, A combination of midazolam and ketamine for procedural sedation and analgesia in adult emergency department patients, <em>Acad Emerg Med<\/em> <strong>7<\/strong> (2000), pp. 228\u0096235. Abstract + References in Scopus | Cited By in Scopus<\/p>\n<p><a href=\"#bbib57\">57<\/a> S.M. Green and J. Li, Ketamine in adults: what emergency physicians need to know about patient selection and emergence reactions [editorial], <em>Acad Emerg Med<\/em> <strong>7<\/strong> (2000), pp. 278\u0096281. Abstract + References in Scopus | Cited By in Scopus<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>RCT of midazolam, NNT of 6 to avoid emergence. They used 0.03 mg\/kg of the midaz (Ann Emerg Med 2011;57:109)<\/p>\n<p>&nbsp;<\/p>\n<p>Ketamine reduces morphine consumption (Am J Emerg Med 2007;25:385)<\/p>\n<p>&nbsp;<\/p>\n<p><strong>Scott Weingart &lt;emcrit@gmail.com&gt; Thu, Jul 17, 2008 at 4:23 AM <\/strong> Reply-To: emcrit@gmail.com To: Scott Weingart &lt;scott.weingart@mssm.edu&gt; Induction phase shoot for 30 minutes 35 no bleeding risk 33.5 coagulopathy \u00a0 \u00a0 PCIM 16 44.1 hz \u00a0 post resus cardioprotective procoagulant ischemic\/reperfusion Ketamine.<\/p>\n<p>Historically, ketamine has played a central role in anesthesia for the trauma patient as a result of the profound analgesia and hemodynamic stability it provides. Increasingly, ketamine has been used for postoperative analgesia and acute pain management in the trauma patient; the Army has for years been interested in developing a nasal formulation of ketamine specifically for acute pain. The Army has accrued significant experience in low-dose ketamine in both acute and chronic pain. Even at subanalgesic doses, it appears to improve fentanyl&#8217;s efficacy in certain pain domains (54, 131).<\/p>\n<p>The most publicized adverse effect of ketamine has been its psychotomimetic effects. Combining ketamine with other agents, such as benzodiazepines or propofol, has been found to attenuate and often abolish the psychotomimetic side effects (132, 133). A series by Friedberg evaluated the use of ketamine, combined with propofol, in 1264 patients premedicated with benzodiazepines and reported no emergence dreams or hallucinations (134). Several studies demonstrate the occurrence of psychotomimetic effects with ketamine is directly related to plasma concentrations of the drug (135, 136). Analgesic plasma concentrations are lower than the plasma concentrations seen with psychotomimetic effects (54, 131).<\/p>\n<p>Long-lasting psychiatric effects have also been a concern surrounding ketamine use. Previous Air Force policy stated that ketamine administration was a nonwaiverable event for flying status. Hersack, in 1994, reviewed the literature for the incidence of long-term side effects and found ketamine had no long-term psychologic effects (137). The only serious sequelae were four cases of psychologic effects lasting up to 3 wks with subsequent resolution. Henceforth, the Air Force changed its policy on ketamine, shortening restricted flying status for the first 3 wks after ketamine administration (137).<\/p>\n<p>A second factor impeding the use of ketamine is purported increases in intracranial pressure (ICP). However, studies supporting this hypothesis were performed in spontaneously ventilating subjects in which the Paco2 was not controlled (138, 139). Research performed in subjects administered ketamine under controlled ventilation demonstrated no evidence of increases in cerebral blood flow or intracranial pressure when CO2 was held constant (140, 141).<\/p>\n<p>Another proposed mechanism of increased ICP secondary to ketamine was a postulated direct dilatory effect on cerebral vasculature (142). Schwedler et al. injected ketamine directly into the cerebral circulation and failed to produce significant change in cerebral blood flow (141). Nonetheless, the current teaching is that ketamine should be avoided in patients with intracranial pathology because it may elevate ICP. When multiple studies enrolling patients with increased ICP were performed, ketamine demonstrated an attenuation of further increases in ICP when administered in combination with a benzodiazepine (143, 144). Patients with traumatic brain injury were also studied, and ketamine demonstrated no adverse effects on cerebral hemodynamics; in fact, decreased ICP was observed in the ketamine group (145).<\/p>\n<p>Another criticism of ketamine is its alleged depressant actions on myocardial tissue, thereby decreasing its use in the patient with a catecholamine-depleted state. This misconception is derived from a study of <em>in vitro<\/em> canine atrial tissue, which demonstrated negative inotropic actions at high plasma concentrations of ketamine (10\u0096300 \u00b5g\/mL) (146). However, clinically used ketamine levels, in the same study (less than 3 \u00b5g\/mL), displayed positive inotropic effects. These early studies also failed to adequately evaluate ketamine&#8217;s cardiovascular action <em>in vivo<\/em> on human subjects at clinically used levels. Many intravenous anesthetics evaluated in human myocardial tissue, including etomidate, propofol, thiopental, and midazolam, found ketamine to be the least depressant on myocardial tissue (147). Ketamine was found to have less negative inotropic effect on the myocardium than etomidate, a widely accepted induction agent for patients with cardiovascular failure. Ketamine is thought to act as a cardiac stimulant through sympathetic-mediated mechanisms.<\/p>\n<p>Cardiac stimulation, however, is not always desired, especially in patients with increased myocardial oxygen demand and limited supply such as those with coronary artery disease. Premedication, especially with benzodiazepines, has been found to reliably attenuate the stimulating cardiovascular effects of ketamine (148). Interestingly, a recent study comparing ketamine with an inhalational\/opioid technique in coronary artery surgery found ketamine use decreased the need for inotropes after surgery and reduced the incidence of myocardial infarctions (149).<\/p>\n<p>Ketamine&#8217;s use throughout the &#8220;inflammatory period&#8221; of injury may result in decreased central hypersensitivity resulting from the continual C fiber windup phenomenon in the polytrauma patient. Ketamine binds noncompetitively to the phencyclidine site of the NMDA receptor as well as sigma opioid receptor resulting in intense analgesia; other benefits include prevention of OIH, decreased opioid tolerance, decreased opioid requirements, increased sense of well-being and patient satisfaction, decreased risk of respiratory depression, and decreased chronic pain. Although anesthetic doses may be associated with secretions as well as agitation and hallucinations, subanesthetic doses are tolerated extremely well with the addition of a benzodiazepine if necessary. The combination of ketamine and morphine in low PCA doses (1 mg morphine and 1 mg ketamine) has been shown to be beneficial with few side effects (150). Ketamine infusions below 2.5 \u00b5g\/kg\/min have also shown similar benefits in reducing opioid consumption and having few side effects (131, 151).<\/p>\n<p>&nbsp;<\/p>\n<p>54. Tucker A, Kim YI, Nadeson R, et al: Investigation of the potentiation of the analgesic effects of fentanyl by ketamine in humans: A double-blinded, randomised, placebo controlled, crossover study of experimental pain. <em>BMC Anesthesiology<\/em> 2005; 5:2 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>55. 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Angst MS, Clark JD: Opioid-induced hyperalgesia: A qualitative systematic review. <em>Anesthesiology<\/em> 2006; 104:570\u0096587 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>59. Celerier E, Rivat C, Jun Y, et al: Long-lasting hyperalgesia induced by fentanyl in rats: Preventive effect of ketamine. <em>Anesthesiology<\/em> 2000; 92:465\u0096472 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>60. Hudcova J, McNicol E, Quah C, et al: Patient controlled opioid analgesia versus conventional opioid analgesia for postoperative pain. <em>Cochrane Database Syst Rev<\/em> 2006; 4:CD003348 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>61. 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A meta-analysis. <em>Anesth Analg<\/em> 2006; 102:248\u0096257 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>65. Schulz-Stubner S, Boezaart A, Hata JS: Regional analgesia in the critically ill. <em>Crit Care Med<\/em> 2005; 33:1400\u00961407 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>66. Pogatzki-Zahn EM, Zahn PK: From preemptive to preventive analgesia. <em>Curr Opin Anaesthesiol<\/em> 2006; 19:551\u0096555 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>67. 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Auroy Y, Benhamou D, Bargues L, et al: Major complications of regional anesthesia in France: The SOS Regional Anesthesia Hotline Service [erratum appears in <em>Anesthesiology<\/em> 2003;98:595 Note: Mercier Frederic {corrected to Mercier Frederic J}]. <em>Anesthesiology<\/em> 2002; 97:1274\u00961280 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>89. Greensmith JE, Murray WB: Complications of regional anesthesia. <em>Curr Opin Anaesthesiol<\/em> 2006; 19:531\u0096537 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>90. Brown DL, Ransom DM, Hall JA, et al: Regional anesthesia and local anesthetic-induced systemic toxicity: seizure frequency and accompanying cardiovascular changes. <em>Anesth Analg<\/em> 1995; 81:321\u0096328 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>91. Foxall G, McCahon R, Lamb J, et al: Levobupivacaine-induced seizures and cardiovascular collapse treated with Intralipid. <em>Anaesthesia<\/em> 2007; 62:516\u0096518 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>92. Litz RJ, Popp M, Stehr SN, et al: Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion. <em>Anaesthesia<\/em> 2006; 61:800\u0096801 <strong>Mount Sinai Serials<\/strong> <strong>Buy Now<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>93. Faccenda KA, Finucane BT: Complications of regional anaesthesia. Incidence and prevention. <em>Drug Saf<\/em> 2001; 24:413\u0096442 <strong>Mount Sinai Serials<\/strong> <strong>Buy Now<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>94. Stan TC, Krantz MA, Solomon DL, et al: The incidence of neurovascular complications following axillary brachial plexus block using a transarterial approach. 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Mini\u00f1o AM, Anderson RN, Fingerhut LA, et al: <em>Increases in Methadone-Related Deaths: 1999\u00962004<\/em>. Statistics NCfH (Ed). Volume 54. Atlanta, Centers for Disease Control and Prevention, 2006 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>109. Center for Substance Abuse Treatment M-AMRoaN, Assessment M-, 2003. <em>SAMHSA Publication No. 04-3904<\/em>. Rockville, MD, Center for Substance Abuse Treatment SAaMHSA, 2004 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>110. Ehret GB, Voide C, Gex-Fabry M, et al: Drug-induced long QT syndrome in injection drug users receiving methadone: High frequency in hospitalized patients and risk factors. <em>Arch Intern Med<\/em> 2006; 166:1280\u00961287 <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>111. Viscusi ER, Reynolds L, Chung F, et al: Patient-controlled transdermal fentanyl hydrochloride vs. intravenous morphine pump for postoperative pain: A randomized controlled trial. <em>JAMA<\/em> 2004; 291:1333\u00961341 <strong>Mount Sinai Serials<\/strong> <strong>Buy Now<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>112. Chelly JE, Grass J, Houseman TW, et al: The safety and efficacy of a fentanyl patient-controlled transdermal system for acute postoperative analgesia: A multicenter, placebo-controlled trial. <em>Anesth Analg<\/em> 2004; 98:427\u0096433 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>113. Walder B, Schafer M, Henzi I, et al: Efficacy and safety of patient-controlled opioid analgesia for acute postoperative pain. 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Koppert W, Schmelz M: The impact of opioid-induced hyperalgesia for postoperative pain. <em>Best Pract Res Clin Anaesthesiol<\/em> 2007; 21:65\u009683 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>121. Remy C, Marret E, Bonnet F: State of the art of paracetamol in acute pain therapy. <em>Curr Opin Anaesthesiol<\/em> 2006; 19:562\u0096565 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>122. Elia N, Lysakowski C, Tramer MR: Does multimodal analgesia with acetaminophen, nonsteroidal antiinflammatory drugs, or selective cyclooxygenase-2 inhibitors and patient-controlled analgesia morphine offer advantages over morphine alone? Meta-analyses of randomized trials. <em>Anesthesiology<\/em> 2005; 103:1296\u00961304 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>123. Dembo G, Park SB, Kharasch ED: Central nervous system concentrations of cyclooxygenase-2 inhibitors in humans. <em>Anesthesiology<\/em> 2005; 102:409\u0096415 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>124. Levesque LE, Brophy JM, Zhang B: The risk for myocardial infarction with cyclooxygenase-2 inhibitors: A population study of elderly adults. <em>Ann Intern Med<\/em> 2005; 142:481\u0096489 <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>125. Grosser T, Fries S, FitzGerald GA: Biological basis for the cardiovascular consequences of COX-2 inhibition: therapeutic challenges and opportunities. <em>J Clin Invest<\/em> 2006; 116:4\u009615 <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>126. Joshi GP: Multimodal analgesia techniques and postoperative rehabilitation. <em>Anesthesiol Clin North Am<\/em> 2005; 23:185\u0096202 <strong>Mount Sinai Serials<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>127. Hayashida K-I, Parker R, Eisenach JC: Oral gabapentin activates spinal cholinergic circuits to reduce hypersensitivity after peripheral nerve injury and interacts synergistically with oral donepezil. <em>Anesthesiology<\/em> 2007; 106:1213\u00961219 [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p>128. Hurley RW, Cohen SP, Williams KA, et al: The analgesic effects of perioperative gabapentin on postoperative pain: A meta-analysis. <em>Reg Anesth Pain Med<\/em> 2006; 31:237\u0096247 <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>129. Bone M, Critchley P, Buggy DJ: Gabapentin in postamputation phantom limb pain: A randomized, double-blind, placebo-controlled, cross-over study. <em>Reg Anesth Pain Med<\/em> 2002; 27:481\u0096486 <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>130. Dirks J, Fredensborg BB, Christensen D, et al: A randomized study of the effects of single-dose gabapentin versus placebo on postoperative pain and morphine consumption after mastectomy. <em>Anesthesiology<\/em> 2002; 97:560\u0096564 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>131. Himmelseher S, Durieux ME: Ketamine for perioperative pain management. <em>Anesthesiology<\/em> 2005; 102:211\u0096220 <strong>Ovid Full Text<\/strong> <strong>Mount Sinai Serials<\/strong> <strong>Bibliographic Links<\/strong> [Context Link]<\/p>\n<p>&nbsp;<\/p>\n<p><a href=\"\/wp-content\/pdf\/hemodynamics%20of%20ketamine.pdf\"> Hemodynamics of ketamine for induction in shock patients<\/a><\/p>\n<p>Neuroleptic doses of droperidol inhibit sympathomimetic effects of ketamine (Anesth and Analg 1983;62(2):193)<\/p>\n<div class=\"cb-section cb-slug\">\n<div id=\"slugline\">\n<p><cite><br \/>\n<abbr class=\"slug-jnl-abbrev\" title=\"Anesthesia &amp; Analgesia\"><br \/>\n<\/abbr><\/cite><\/p>\n<\/div>\n<\/div>\n<h4><strong>Cardiac Dysfunction<\/strong><\/h4>\n<p><a title=\"Anaesthesia and intensive care.\"> Anaesth Intensive Care.<\/a>\u00a01997 Jun;25(3):255-9<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p><strong>Failure to successfully complete a procedure following emergency department sedation<\/strong>DMcD Taylor1,2 for the Emergency Department Sedation Study Investigators1Austin Health; 2University of Melbourne, Melbourne, Australia<\/p>\n<p><em>Aims:<\/em> To determine the nature and incidence of, and factors contributing to, failure to successfully complete a procedure fol- lowing sedation in the ED<\/p>\n<p><em>Methods<\/em>: Eleven Australian ED enrolled consecutive adult and paediatric patients between January 2006 and December 2008. Patients were included if a sedative drug was administered for an ED procedure. Data collection was prospective and employed a specifically designed form.<\/p>\n<p><em>Results<\/em>: Two thousand six hundred and twenty three patients were enrolled (60.3% male, mean age 39.2 years). Failure to successfully complete the procedure occurred in 148 (5.6%) cases. Most failures occurred with attempted reductions of fractured\/dislocated shoulders (35 cases), hips (32), ankles (21) and elbows (14). However, failure rates were highest among fractured\/dislocated hips (18.5%), digits (13.7%), femurs (11.1%), mandibles (10.2%) and elbows (9.3%). Failure rates for residents\/registrars (5.9%), consultants (5.6%) and nurse practitioners (5.9%) did not differ (P = 0.92). Overall, failure rates for the various drugs (used alone or in combina- tion) did not differ (P = 0.07). However, ketamine (used alone or in combination) was associated with a much lower failure rate (2.9%) than all other sedation drugs used (midazolam 5.8%, propofol 6.5%, fentanyl 6.9%, nitrous oxide 7.1%, and morphine 7.8%).<\/p>\n<p><em>Conclusion<\/em>: Procedural failure is uncommon although some pro- cedures are at higher risk, especially dislocated hip reduction. Failure rates do not appear to be affected by the designation of the operator or the sedative drug used. However, ketamine use is associated with lower failure rates. For those procedures at higher risk of failure, the provision of optimal conditions (spe- cialist unit assistance, venue, drug selection) may minimise failure rates.<\/p>\n<p>Emergency Medicine Australasia 2010;22(S1):A52-3<\/p>\n<p>The cardiorespiratory patterns of critically ill patients brought to the ORand induced with Ketamine. It seems any hypertension is from increased CO and not from increased SVR to any sig. extent. (Crit Care Med 1983;11(9):730)<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Ketofol\"><\/span>Ketofol<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Ketofol (1:1 mixture of ketamine 10 mg\/mL and propofol 10 mg\/mL) was administered intravenously at the discretion of the treating physician by using titrated aliquots. [Ann Emerg Med. 2007;49:23-30.]<\/p>\n<p>&nbsp;<\/p>\n<p>no real benefits over propofol alone (Ann Emerg Med 2011;57:435)<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Etomidate\"><\/span>Etomidate<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>.1 mg\/kg Etomidate up to three doses with fentanyl (Annals EM 40:5, 2002)<\/p>\n<p>others use .15 mg\/kg x 2 or go right with .3 mg\/kg<\/p>\n<p>Consider combo of fentanyl and droperidol (INNOVAR)<\/p>\n<p>&nbsp;<\/p>\n<p>(4) Dursteler BB, et al. Etomidate-facilitated hip reduction in the emergency department Acad Emerg Med 2000;7: 1165-6. (5) Frymann SJ, et al. Reduction of dislocated hip prosthesis in the emergency department using conscious sedation: a prospective study Emergency Medicine Journal 2005;22:807-809<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>low dose versed (0.015 mg\/kg) given 90 sec before etomidate attenuates the myoclonus and doesn&#8217;t prolong time to recovery. (Anesth Analg 2007;105:1298)<\/p>\n<p>&nbsp;<\/p>\n<p>The question of ketamine &#8220;flashbacks&#8221; is valid as ketamine is a phencyclidine related to lysergic acid (LSD). Ketamine interferes with the formation of long-term memory at the level of the hippocampus and can thus generate delusionalmemories that are the basis of &#8220;flashbacks&#8221;. However this requires the generation of a previous short-term memory that is inhibited by co- administration of a GABA agonist, most commonly midazolam. My commonest mix is ketamine 50 mg (5ml of 10mg\/ml) and midazolam 5mg (5ml of 1mg\/ml). A 2ml initial bolus followed by 1ml every 5-10 min will provide comfort for a wide variety of procedures with no risk of long term effects and very reliable amnesia.<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Propofol\"><\/span>Propofol<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Add 30 mg of ephedrine to each 20 cc of propofol for decreased pain of injection and better hemodynamic profile (J Clin Anesth 2009;21:44)<\/p>\n<p>Preloading with fluids doesn&#8217;t prevent BP drop (Intensive Care Med (2013) 39:1377\u20131385)<\/p>\n<p>Initial bolus: Various Guidelines say 0.5 to 2 mg \/ kg bolus. I would recommend sticking with the lower end 0.5-1 mg\/kg To make it even easier just give 50 mg bolus to an average size adult; The recommendations on drip rates are all over the place ranging from 10 mcg\/kg\/min to 200 mcg\/kg\/min. I think 10 mcg\/kg\/ min is too low and a more reasonable starting dose is 100 mcg\/kg\/min and then titrate upwards by 20 mcg\/kg\/min every 5 min. I saw one protocol by GI docs for colonoscopy which started at 140 mcg\/kg\/min. If they can started at 140 mcg\/kg\/min without complications then I feel confident that our ED docs can start at 100 mcg\/kg\/min and deliver safe sedation. So to summarize give 0.5-1 mg\/kg bolus (50 mg is fine for most adults) followed by a drip at 100 mcg\/kg\/min. Titrate upward by 20 mcg\/kg\/min q 5 min.<\/p>\n<p><strong>Soybean oil and egg lecithin <\/strong>are components of the emulsion that contains propofol. \u00a0Hypersensitivity to these components or the drug itself contraindicates use of the drug as presently formulated. Allergy to eggs alone, is probably safe (<\/p>\n<p>&nbsp;<\/p>\n<p><span id=\"article-slug-jnl-abbr\"><br \/>\n<abbr class=\"slug-jnl-abbrev\" title=\"Emergency Medicine Journal\"><br \/>\nEmerg Med J<\/abbr><br \/>\n<\/span><br \/>\n<span class=\"slug-pub-date\">2013;<\/span><span class=\"slug-vol\">30<span class=\"cit-sep cit-sep-after-article-vol\">:<\/span><\/span><span class=\"slug-pages\">79-80<\/span>)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>(Academic EM 10:9 931-937, Sept 2003) Randomized Clinical Trial of Propofol versus Methohexital for Procedural Sedation during Fracture and Dislocation Reduction in the Emergency Department:\u00a0 1 mg\/kg then 0.5 mg\/kg Q 3-5 minutes<\/p>\n<p>Propofol (2,6-diisopropylphenol), an oil in water emulsion, is an intravenous agent that is used for induction and maintenance of anesthesia.7 Propofol, like benzodiazepines, inhibits activity at both the spinal and supraspinal synapses by interacting with and potentiating the GABA-mediated receptors.8,9 However, it does not potentiate GABA-evoked currents through the benzodiazepine site.10 When combined with flurazepam, the potentiation of GABA receptor activity obtained with propofol is greater than expected from a simple additive response.<\/p>\n<p>&nbsp;<\/p>\n<p>Intravenous injection of propofol produces a rapid hypnosis, usually by 40 seconds after the start of a bolus injection. Maintenance of sedation (25 to 75 \u00b5g\/kg\/minute) or anesthesia (100 to 200 \u00b5g\/kg\/minute) can be achieved by continuous intravenous infusion titrated to clinical effect.7 Propofol distributes very rapidly throughout the body including the brain. The pharmacokinetic profile of propofol is described by a three-compartment model:<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Propofol_Infusion_Syndrome\"><\/span><a href=\"https:\/\/crashingpatient.com\/toxicology\/general-toxicology-random-drugs.htm\/\">Propofol Infusion Syndrome<\/a><span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Sedation_for_Cardioversion_Study\"><\/span>Sedation for Cardioversion Study<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>(Annals EM Dec 2003 42:6)<\/p>\n<p>Propofol (9) vs. Etomidate (9) vs. Midazolam (8) vs. Midazolam with flumazenil (6)<\/p>\n<p>Recovery Etomidate 9.5 minutes, Midazolam 21 minutes, Propofol 8 minutes, Midaz c flumaz 3 minutes but high resedation rate<\/p>\n<p>Flumaz protocol was .5 mg bolus then .5 mg over one hour<\/p>\n<p>Etomidate .2 mg\/kg<\/p>\n<p>Propofol 1.5 mg\/kg<\/p>\n<p>Midazolam .2 mg\/kg<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Hemodynamic effects of propofol sedation (Anesthesiology 2005;103:20)<\/p>\n<p>It has substantial inhibitory effects on sympathetic activity and reflex responses to hypotension<\/p>\n<p>this causes vasodilation and decreased MAP<\/p>\n<p>&nbsp;<\/p>\n<p>Study using infusion instead of injection (Am J Emerg Med. 2006 Sep;24(5):599-602)<\/p>\n<p>Because of propofol&#8217;s lack of analgesic activity, fentanyl was given intravenously at a dose of 2 \u03bcg\/kg approximately 2 minutes before beginning the propofol infusion. Propofol was then begun as an infusion using a pump. Initially, a loading infusion of 0.21 mg kg\u22121 min\u22121 was given until the patient was sedated to an appropriate level, assessed by the attending emergency physician. At this point, the procedure was started, and the propofol infusion was switched to a maintenance rate of 3-6 mg kg\u22121 h\u22121, at the attending physician&#8217;s discretion, until the procedure was completed. A table with appropriate doses and drip rates was compiled and available at all times during the procedure Etomidate and propofol appear equally safe for ED procedural sedation; however, etomidate had a lower rate of procedural success and induced myoclonus in 20% of patients. (Annals of Emergency Medicine\u00a0 Volume 49, Issue 1 , January 2007, Pages 15-22) Anaesthesia Volume 62 Issue 7 Page 690Issue 7 &#8211; 701 &#8211; July 2007 To cite this article: P. C. A. Kam, D. Cardone (2007) Propofol infusion syndrome Propofol infusion syndrome (Anaesthesia 62 (7), 690\u0096701.)<\/p>\n<p>&nbsp;<\/p>\n<p>We read with interest the recent correspondence highlighting the inclusion of peanut allergy in the list of contra-indications in the product literature for propofol [<a>1<\/a>]. The potential for peanut-allergic patients to be sensitive to propofol is due to the fact that soya oil is one of the excipients of propofol, and that cross-reactivity occurs in legume allergy, for example between soya and peanut. However, it is the protein component that is responsible for allergic reactions in these patients, and as the soya oil present in propofol is refined, it is unlikely to contain significant quantities of allergenic particles. In the food industry soya-containing mixed vegetable oil may be sold for consumption without listing soya as an ingredient [<a>2<\/a>]. The reason for this is that the dose of protein contained in refined soya oil is too small to provoke a reaction when ingested. Although the minimum dose of protein required to trigger a reaction after oral ingestion has been identified, the same is not true of parenteral administration [<a>3<\/a>].<\/p>\n<p>There is no mention of egg allergy in the product literature for propofol. The main triggers for egg anaphylaxis are three proteins found in egg white: ovoalbumin, ovomucoid and conalbumin. Lecithin, a purified egg phosphatide present in propofol, is not thought to be problematic for patients who are allergic to eggs. Allergic reactions to propofol have been shown to be triggered by the iso-propyl or phenol groups rather than the lipid vehicle [<a>4, 5<\/a>].<\/p>\n<p>One case report describes an anaphylactic reaction following administration of propofol to a child with multiple food allergies including egg and peanut. However, other drugs including rocuronium had also been administered. Skin prick testing was not performed and the specific causative agent remains unclear [<a>6<\/a>]. We have spoken to the Medical Information Department at AstraZeneca who informed us that the final decision to use Diprivan in patients with egg allergy remains at the discretion of the individual anaesthetist concerned (personal communication, D. Gupta, AstraZeneca Ltd).<\/p>\n<p>In summary, the negligible protein content of refined soya oil in propofol suggests the drug is unlikely to trigger a reaction in patients with peanut allergy. The fact that the product literature cites this as a contra-indication must, however, be given careful consideration prior to administration. If the clinician decides propofol is unsuitable, inhalational induction of anaesthesia may provide a useful alternative.<\/p>\n<p>&nbsp;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Xenon\"><\/span>Xenon<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>May have potential as an inhalational sedative without hemodynamic side effects (Crit Care Med 2003 31:10)<\/p>\n<p>&nbsp;<\/p>\n<p>We can sedate the critically ill, unstable patient (Acad Emerg Med 2005;12(2):124)<\/p>\n<p>&nbsp;<\/p>\n<p>0.5 mg\/kg of propofol plus 0.5\u00b5g\/kg of remifentanil, given intravenously over 60 and30 seconds, respectively for shoulder dislocation (EMJ 2006;23:57-58)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>capnography for procedural sedation (Ann Emerg Med 2007;50:172) \u00a0 review of propofol sedation (Ann Emerg Med 2007;50:182)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Flumazenil<\/p>\n<p>clinical effects 30-60 min duration<\/p>\n<p>0.5-5 mg infused over 3-5 min<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Propofol-2\"><\/span>Propofol<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>avoid using in egg, soybean, or EDTA allergy<\/p>\n<p>interacts with GABA receptor system<\/p>\n<p>prolongs duration of contact between gaba and its receptor site<\/p>\n<p>liver metabolized<\/p>\n<p>duration ~8 minutes<\/p>\n<p>antiemetic qualities<\/p>\n<p>rapid IV bolus causes higher incidence of resp depression<\/p>\n<p>ketamine\/propofol combination may mitigate the cardiovascular effects<\/p>\n<p>cat b in pregnancy<\/p>\n<p>0.5 mg\/kg of lidocaine mixed up with propofol will limit pain on injection<\/p>\n<p>&nbsp;<\/p>\n<p>for sedation consider giving 10% of induction (1.5 mg\/kg) dose<\/p>\n<p>&nbsp;<\/p>\n<p>ketamine + propofol<\/p>\n<p>5 mg\/cc solution of each titrate 1-2 cc at a time<\/p>\n<p>can be placed in the same syringe<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Etomidate-2\"><\/span>Etomidate<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>premed with opioids or benzos may decrease myoclonus<\/p>\n<p>or you can use magnesium The following article reported decreased myoclonus with Mg++ pretreatment. I believe the authors used 100 mg Mg++. I have found that 300-500 mg seems to work better with younger patients and higher doses of etomidate. There may still be a small amount of twitching, but greatly reduced.Anesth Analg 2005;101:705-709<\/p>\n<p>use with lidocaine to decrease injection burning<\/p>\n<p>ADD lidocaine to sedation checklist<\/p>\n<p>inhibition of gaba neurotransmission<\/p>\n<p>redistribution from brain to peripheral tissues accounts for its short action, though eventual metabolism is by liver<\/p>\n<p>1\/3 of patients will have myoclonus<\/p>\n<p>dantrolene 1mg\/kg can terminate severe myoclonus<\/p>\n<p>propylene glycol is diluent<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Ketamine-2\"><\/span><strong>Ketamine <\/strong><span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>no pain on injection<\/p>\n<p>now known pretreatment with benzos has no benefit<\/p>\n<p>include fall precautions on d\/c instructions<\/p>\n<p>inhibits gaba, halmoneocortical projection system, NDMA and mu agonist<\/p>\n<p>&nbsp;<\/p>\n<p>arylcyclohexylamine resembling PCP<\/p>\n<p>liver metabolized<\/p>\n<p>increases cardiac output<\/p>\n<p>benzos delay ketamine metabolism prolonging action<\/p>\n<p>cat B in pregnancy (though sources have various listings)<\/p>\n<p>1.5 mg\/kg, IM dosing is 4 mg\/kg<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Benzodiazepenes\"><\/span>Benzodiazepenes<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>nitroglycerin like effect on heart fx paitents which reduces ventricular filling<\/p>\n<p>hepatic p450 metabolism<\/p>\n<p>increase frequency of cl channel opening<\/p>\n<p>ativan and versed essentially have the same dosing with 2 of either = to about 5 of valium<\/p>\n<p>ativan has no active metabolites, diazepam and versed do. Kidney fx will cause prolonged action<\/p>\n<p>paradoxical agitation<\/p>\n<p>class D in pregnancy<\/p>\n<p>Frequent hypoxemia and apnea after sedation with midazolam and fentanyl (Anesthesiology 1990;73:826) Midazolam alone had no resp depressant effects. Fentanyl alone produced hypoxemia but not apnea. Midaz + fentanyl had sig. increased rate of hypoxemia.<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"ETCO2\"><\/span>ETCO2<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>ETCO2 monitoring makes procedural sedation safer (<em>Acad Emerg Med<\/em> Volume 13, Number 5 500-504)<\/p>\n<p>&nbsp;<\/p>\n<p>Meta-Analysis of capnography during procedural sedation (J Clin Anesth 2011;23:189)<\/p>\n<p>17.6 x more likely to detect resp depression if ETCO2 is used<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Supplemental_Oxygen\"><\/span>Supplemental Oxygen<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: 400; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\"><span style=\"border-collapse: separate; color: #000000; font-family: Tahoma; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px; font-size: medium;\">They summarise:<\/span><\/p>\n<p><span style=\"border-collapse: separate; color: #000000; font-family: Tahoma; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px; font-size: medium;\"><em style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: italic; font-variant: normal; font-weight: 400; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">\u201c\u2026assuming that capnography is in place to monitor ventilatory function, our results strongly support the routine use of high-flow oxygen during ED propofol sedation\u201d<\/em><\/span><\/p>\n<blockquote style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: 400; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\"><p><span style=\"border-collapse: separate; color: #000000; font-family: Tahoma; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px; font-size: medium;\"><br clear=\"none\" \/><strong style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: bold; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">STUDY OBJECTIVE:<\/strong>\u00a0We determine whether high-flow oxygen reduces the incidence of hypoxia by 20% in adults receiving propofol for emergency department (ED) sedation compared with room air.<br clear=\"none\" \/><br clear=\"none\" \/><strong style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: bold; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">METHODS:\u00a0<\/strong>We randomized adults to receive 100% oxygen or compressed air at 15 L\/minute by nonrebreather mask for 5 minutes before and during propofol procedural sedation. We administered 1.0 mg\/kg of propofol, followed by 0.5 mg\/kg boluses until the patient was adequately sedated. Physicians and patients were blinded to the gas used. Hypoxia was defined a priori as an oxygen saturation less than 93%; respiratory depression was defined as an end tidal CO(2) greater than 50 mm Hg, a 10% absolute change from baseline, or loss of waveform.<br clear=\"none\" \/><br clear=\"none\" \/><strong style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: bold; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">RESULTS:\u00a0<\/strong>We noted significantly less hypoxia in the 59 patients receiving high-flow oxygen compared with the 58 receiving compressed air (19% versus 41%; P=.007; difference 23%; 95% confidence interval 6% to 38%). Respiratory depression was similar between groups (51% versus 48%; difference 2%; 95% confidence interval -15% to 22%). We observed 2 adverse events in the high-flow group (1 hypotension, 1 bradycardia) and 2 in the compressed air group (1 assisted ventilation, 1 hypotension).<br clear=\"none\" \/><br clear=\"none\" \/><strong style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: bold; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">CONCLUSION:\u00a0<\/strong>High-flow oxygen reduces the frequency of hypoxia during ED propofol sedation in adults.<br clear=\"none\" \/><br clear=\"none\" \/><\/span><\/p><\/blockquote>\n<p style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: 400; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\"><strong style=\"color: #202020; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: bold; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\">The Utility of High-Flow Oxygen During Emergency Department Procedural Sedation and Analgesia With Propofol: A Randomized, Controlled Trial<\/strong><br clear=\"none\" \/><a style=\"color: #4747c5; font-family: Arial,Tahoma,Verdana; font-size: 12px; font-style: normal; font-variant: normal; font-weight: 400; text-align: start; text-decoration: none; text-indent: 0px; text-shadow: none; text-transform: none; color-interpolation: srgb; color-interpolation-filters: linearrgb; text-anchor: start; text-rendering: auto;\" href=\"http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/21680059\" target=\"_blank\" shape=\"rect\">Ann Emerg Med. 2011 Oct;58(4):360-364<\/a><\/p>\n<h2><span class=\"ez-toc-section\" id=\"When_to_Discharge\"><\/span>When to Discharge<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p><a href=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/sampledcinstructions1.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-thumbnail wp-image-8472\" title=\"sampledcinstructions\" src=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/sampledcinstructions1-150x150.png\" alt=\"\" width=\"150\" height=\"150\" \/><\/a><a href=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/whentoterminate.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-thumbnail wp-image-8473\" title=\"whentoterminate\" src=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/whentoterminate-150x150.png\" alt=\"\" width=\"150\" height=\"150\" \/><\/a><a href=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/dischargescores.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-thumbnail wp-image-8474\" title=\"dischargescores\" src=\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/07\/dischargescores-150x150.png\" alt=\"\" width=\"150\" height=\"150\" \/><\/a><\/p>\n<h2><span class=\"ez-toc-section\" id=\"Remifentanil\"><\/span>Remifentanil<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>remifentanil review article<\/p>\n<p>&nbsp;<\/p>\n<p>Hyperoxia exacerbates opioid-induced resp depression (Br. J. Anaesth. (2013) 110 (5): 837-841.)<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"NIPPV\"><\/span>NIPPV<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>from Strayer et al (Am J Emerg Med 2015;33:108)<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[39],"tags":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v22.5 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Procedural Sedation - Crashing Patient<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/crashingpatient.com\/resuscitation\/sedation\/procedural-sedation.htm\/\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"CrashMaster\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"40 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\/\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\/\/crashingpatient.com\/resuscitation\/sedation\/procedural-sedation.htm\/\",\"url\":\"https:\/\/crashingpatient.com\/resuscitation\/sedation\/procedural-sedation.htm\/\",\"name\":\"Procedural Sedation - 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