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MAC Reduction

2010-09-06T19:42:05Z

Enoxaparin: assessment of effect

2010-09-06T19:18:55Z

←Older revision		Revision as of 19:18, 6 September 2010
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-	~~Low~~ molecular weight heparin (LMWH) ~~enhances~~ the ~~ability~~ of ~~Antithrombin~~ to ~~proteolytically inactivate~~ activated ~~Factor X~~ (~~Factor Xa~~). ~~The PT~~ and ~~PTT are not useful~~ for monitoring LMWH. The ~~only reliable way~~ is with an anti-~~Factor~~ Xa ~~level~~. The ~~higher~~ the LMWH, the ~~lower~~ the ~~level~~ of ~~Factor~~ Xa. ~~This inverse relationship~~ is ~~calculated~~ and ~~converted~~ to anti-Xa ~~units~~. ~~This should~~ be ~~drawn~~ 4 hours ~~after~~ the ~~second or third dose~~. ~~No prospective~~ therapeutic range trials ~~were performed~~ and ~~recommendations are controversial~~. ~~Most~~ patients do not ~~require monitoring~~, ~~but~~ it may ~~be warranted~~ for ~~those~~ on ~~recent~~ or ~~concurrent anticoagulation~~ or a ~~condition indicating~~ a ~~high~~ risk of bleeding.	+	Enoxaparin, like any LMWH, is derived by depolymerization of unfractionated heparin and retains UFH’s ability to activate antithrombin and thereby provide anticoagulation. Largely secondary to its smaller molecular size, enoxaparin binds less to plasma proteins, macrophages, and endothelial cells, thereby promoting a '''more reliable dose-response relationship and longer plasma half-life''' compared to UFH. [<balloon title="This article about unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) is part of the Seventh American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy: Evidence-Based Guidelines. UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors. UFH also binds endothelial cells, platelet factor 4, and platelets, leading to rather unpredictable pharmacokinetic and pharmacodynamic properties. Variability in activated partial thromboplastin time (aPTT) reagents necessitates site-specific validation of the aPTT therapeutic range in order to properly monitor UFH therapy. Lack of validation has been an oversight in many clinical trials comparing UFH to LMWH. In patients with apparent heparin resistance, anti-factor Xa monitoring may be superior to measurement of aPTT. LMWHs lack the nonspecific binding affinities of UFH, and, as a result, LMWH preparations have more predictable pharmacokinetic and pharmacodynamic properties. LMWHs have replaced UFH for most clinical indications for the following reasons: (1) these properties allow LMWHs to be administered subcutaneously, once daily without laboratory monitoring; and (2) the evidence from clinical trials that LMWH is as least as effective as and is safer than UFH. Several clinical issues regarding the use of LMWHs remain unanswered. These relate to the need for monitoring with an anti-factor Xa assay in patients with severe obesity or renal insufficiency. The therapeutic range for anti-factor Xa activity depends on the dosing interval. Anti-factor Xa monitoring is prudent when administering weight-based doses of LMWH to patients who weigh greater than 150 kg. It has been determined that UFH infusion is preferable to LMWH injection in patients with creatinine clearance of less than 25 mL/min, until further data on therapeutic dosing of LMWHs in renal failure have been published. However, when administered in low doses prophylactically, LMWH is safe for therapy in patients with renal failure. Protamine may help to reverse bleeding related to LWMH, although anti-factor Xa activity is not fully normalized by protamine. The synthetic pentasaccharide fondaparinux is a promising new antithrombotic agent for the prevention and treatment of venous thromboembolism." style="color:green">Hirsh J Chest 126 (3S): 188S, 2004</balloon> [http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=15383472 FREE Full Text]]
		+
		+	'''Compared to UFH, enoxaparin has lower anti-IIa activity relative to anti-Xa activity''' and this translates into a reduced effect on the aPTT. '''The increase in the aPTT observed with UFH is largely due to its anti-IIa activity'''. Because of its more predicable pharmacokinetics, enoxaparin is given in fixed doses for thromboprophylaxis and total body weight (TBW)-adjusted doses for full anticoagulation, typically without laboratory monitoring. [<balloon title="This article about unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) is part of the Seventh American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy: Evidence-Based Guidelines. UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors. UFH also binds endothelial cells, platelet factor 4, and platelets, leading to rather unpredictable pharmacokinetic and pharmacodynamic properties. Variability in activated partial thromboplastin time (aPTT) reagents necessitates site-specific validation of the aPTT therapeutic range in order to properly monitor UFH therapy. Lack of validation has been an oversight in many clinical trials comparing UFH to LMWH. In patients with apparent heparin resistance, anti-factor Xa monitoring may be superior to measurement of aPTT. LMWHs lack the nonspecific binding affinities of UFH, and, as a result, LMWH preparations have more predictable pharmacokinetic and pharmacodynamic properties. LMWHs have replaced UFH for most clinical indications for the following reasons: (1) these properties allow LMWHs to be administered subcutaneously, once daily without laboratory monitoring; and (2) the evidence from clinical trials that LMWH is as least as effective as and is safer than UFH. Several clinical issues regarding the use of LMWHs remain unanswered. These relate to the need for monitoring with an anti-factor Xa assay in patients with severe obesity or renal insufficiency. The therapeutic range for anti-factor Xa activity depends on the dosing interval. Anti-factor Xa monitoring is prudent when administering weight-based doses of LMWH to patients who weigh greater than 150 kg. It has been determined that UFH infusion is preferable to LMWH injection in patients with creatinine clearance of less than 25 mL/min, until further data on therapeutic dosing of LMWHs in renal failure have been published. However, when administered in low doses prophylactically, LMWH is safe for therapy in patients with renal failure. Protamine may help to reverse bleeding related to LWMH, although anti-factor Xa activity is not fully normalized by protamine. The synthetic pentasaccharide fondaparinux is a promising new antithrombotic agent for the prevention and treatment of venous thromboembolism." style="color:green">Hirsh J Chest 126 (3S): 188S, 2004</balloon> [http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=15383472 FREE Full Text]] However, '''since LMWHs are renally-cleared, their half-life is prolonged in renal insufficiency'''. Additionally, dose-adjustment of enoxaparin can be troublesome in severely obese patients. Based on these observations, laboratory monitoring of LMWH has been advised in such situations, particularly when weight-based regimens are used.
		+
		+	'''Anti-Xa activity monitoring by a chromogenic assay is the most widely available and the test recommended by the College of American Pathologists for this purpose.''' Following a therapeutic weight-based dose of enoxaparin given subcutaneously, the anti-Xa activity peaks at 4 hours and this is the advised time to conduct monitoring assays.[<balloon title="This article about unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) is part of the Seventh American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy: Evidence-Based Guidelines. UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors. UFH also binds endothelial cells, platelet factor 4, and platelets, leading to rather unpredictable pharmacokinetic and pharmacodynamic properties. Variability in activated partial thromboplastin time (aPTT) reagents necessitates site-specific validation of the aPTT therapeutic range in order to properly monitor UFH therapy. Lack of validation has been an oversight in many clinical trials comparing UFH to LMWH. In patients with apparent heparin resistance, anti-factor Xa monitoring may be superior to measurement of aPTT. LMWHs lack the nonspecific binding affinities of UFH, and, as a result, LMWH preparations have more predictable pharmacokinetic and pharmacodynamic properties. LMWHs have replaced UFH for most clinical indications for the following reasons: (1) these properties allow LMWHs to be administered subcutaneously, once daily without laboratory monitoring; and (2) the evidence from clinical trials that LMWH is as least as effective as and is safer than UFH. Several clinical issues regarding the use of LMWHs remain unanswered. These relate to the need for monitoring with an anti-factor Xa assay in patients with severe obesity or renal insufficiency. The therapeutic range for anti-factor Xa activity depends on the dosing interval. Anti-factor Xa monitoring is prudent when administering weight-based doses of LMWH to patients who weigh greater than 150 kg. It has been determined that UFH infusion is preferable to LMWH injection in patients with creatinine clearance of less than 25 mL/min, until further data on therapeutic dosing of LMWHs in renal failure have been published. However, when administered in low doses prophylactically, LMWH is safe for therapy in patients with renal failure. Protamine may help to reverse bleeding related to LWMH, although anti-factor Xa activity is not fully normalized by protamine. The synthetic pentasaccharide fondaparinux is a promising new antithrombotic agent for the prevention and treatment of venous thromboembolism." style="color:green">Hirsh J Chest 126 (3S): 188S, 2004</balloon> [http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=15383472 FREE Full Text]] A conservative therapeutic range for peak effect with BID dosing of enoxaparin is 0.6-1.0 IU/mL for patients being treated for venous thromboembolism. In order to avoid an increased risk of bleeding, levels of >1 IU/mL should be avoided in patients with renal insufficiency or severe obesity.
		+
		+	Since intravascular volume and volume of distribution does not have a linear relationship with TBW, it has been thought that weight based regimens of LMWH for obese patients may lead to overdosing. Interestingly, anti-Xa activity is not significantly increased when LMWH is given to obese patients based on TBW. Additionally, an increased rate of bleeding is not seen with weight-based regimens. However, since few studies have included patients exceeding 150 kg and BMI > 50, it is reasonable to perform anti-Xa monitoring in such patients due to the above theoretical concerns.
		+
		+	'''The clearance of LMWH is directly proportional to the creatinine clearance (CrCl)'''. The administration of multiple therapeutic doses of enoxaparin has been shown to result in significantly elevated anti-Xa levels in subjects with CrCl under 30 mL/min. Renal insufficiency has been shown to increase the risk of major bleeding complications following therapeutic anticoagulation with LMWH. In one large study, '''a CrCl < 30mL/min was associated with increased incidence of major hemorrhage in patients treated with enoxaparin''' [<balloon title="BACKGROUND: The advantages of enoxaparin over unfractionated heparin (UFH) for the treatment of patients with non-ST-segment elevation acute coronary syndromes are well established. However, no data are available about the safety and efficacy in patients who are obese and patients with severe renal impairment. METHODS: A retrospective analysis of treatment effects was performed on patients who were obese and patients with severe renal impairment from the Efficacy Safety Subcutaenous Enoxaparin in Non-Q-wave Coronary Events (ESSENCE) and Thrombolysis in Myocardial Infarction (TIMI) 11B trials, in which patients were treated with enoxaparin or UFH. The primary composite end point was death, myocardial infarction (MI), and urgent revascularization (UR), and the secondary end points were major and any hemorrhage. RESULTS: When compared with UFH, enoxaparin reduced the rate of the primary end point in patients who were obese (14.3% vs 18.0%, P =.05), patients who were not obese (16.1% vs 19.2%, P less than .01), and patients without severe renal impairment (15.7% vs 18.4%, P less than .01). There was no significant difference in major bleeding between enoxaparin and UFH in any of the 4 subgroups. There were no differences in either the primary end point (17.6% vs 16.2%, P =.39) or major hemorrhage (1.3% vs 0.8%, P =.12) in patients who were obese receiving either UFH or enoxaparin compared with patients who were not obese. Patients with severe renal impairment tended toward a higher rate of the primary end point (25.9% vs 17%, P =.09) and experienced more major hemorrhages (6.6% vs 1.1%, P less than .0001). CONCLUSIONS: Enoxaparin reduced the rate of the combined end point of death/MI/UR in the subgroups of patients who were obese, patients who were not obese, and patients without renal insufficiency. Obesity did not impact clinical outcomes in the combined analysis of ESSENCE and TIMI 11B. Patients with severe renal impairment have a higher risk of clinical events and major and any hemorrhages than patients without severe renal impairment, whether they are treated with UFH or enoxaparin." style="color:green">Spinler S Am Heart J 146: 33, 2003</balloon>]. Based on this, '''UFH should be the first choice agent for therapeutic anticoagulation for patients with CrCl under 30 mL/min. If enoxaparin must be used, anti-Xa levels should be obtained to guide therapy'''. [<balloon title="This article about unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) is part of the Seventh American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy: Evidence-Based Guidelines. UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors. UFH also binds endothelial cells, platelet factor 4, and platelets, leading to rather unpredictable pharmacokinetic and pharmacodynamic properties. Variability in activated partial thromboplastin time (aPTT) reagents necessitates site-specific validation of the aPTT therapeutic range in order to properly monitor UFH therapy. Lack of validation has been an oversight in many clinical trials comparing UFH to LMWH. In patients with apparent heparin resistance, anti-factor Xa monitoring may be superior to measurement of aPTT. LMWHs lack the nonspecific binding affinities of UFH, and, as a result, LMWH preparations have more predictable pharmacokinetic and pharmacodynamic properties. LMWHs have replaced UFH for most clinical indications for the following reasons: (1) these properties allow LMWHs to be administered subcutaneously, once daily without laboratory monitoring; and (2) the evidence from clinical trials that LMWH is as least as effective as and is safer than UFH. Several clinical issues regarding the use of LMWHs remain unanswered. These relate to the need for monitoring with an anti-factor Xa assay in patients with severe obesity or renal insufficiency. The therapeutic range for anti-factor Xa activity depends on the dosing interval. Anti-factor Xa monitoring is prudent when administering weight-based doses of LMWH to patients who weigh greater than 150 kg. It has been determined that UFH infusion is preferable to LMWH injection in patients with creatinine clearance of less than 25 mL/min, until further data on therapeutic dosing of LMWHs in renal failure have been published. However, when administered in low doses prophylactically, LMWH is safe for therapy in patients with renal failure. Protamine may help to reverse bleeding related to LWMH, although anti-factor Xa activity is not fully normalized by protamine. The synthetic pentasaccharide fondaparinux is a promising new antithrombotic agent for the prevention and treatment of venous thromboembolism." style="color:green">Hirsh J Chest 126 (3S): 188S, 2004</balloon> [http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=15383472 FREE Full Text]]
		+
		+	[[Category: ABA Keywords]]

Epidural clonidine: mechanism of action

2010-09-06T19:03:34Z

New page: Clonidine functions as a sympatholytic by stimulating presynaptic α2-receptors leading to decreased release of norepinephrine at both central and peripheral adrenergic terminals. In addi...

New page

Clonidine functions as a sympatholytic by stimulating presynaptic α2-receptors leading to decreased release of norepinephrine at both central and peripheral adrenergic terminals. In addition to its influence on the autonomic nervous system, it is well established that clonidine is an effective analgesic, and this is also attributable to its α2-agonist activity.
 
Remember that '''a tremendous amount of modulation of incoming pain signals occurs in the dorsal horn of the spinal cord prior to being sent to higher centers in the CNS'''. Messages are either strengthened or attenuated by release of various neurotransmitters by primary afferent Aδ or C fibers, interneurons, and descending bulbospinal fibers. Nociceptive stimuli will promote release of excitatory transmitters from primary afferents in the dorsal horn. To compensate, '''there is simultaneous release of norepinephrine from descending inhibitory bulbospinal neurons, which binds to α2-receptors in the dorsal horn to diminish afferent pain transmission, thereby producing analgesia'''. [http://www.eurosiva.org/Archive/Nice/SpeakerAbstracts/Chiari.htm Chiari, Astrid. Neostigmine and Alpha-2 Agonists as Additives for Neuraxial Blockade January 2000]
 
It is logical, therefore, that drugs targeting α2-receptors should influence the transmission and perception of pain. Cocaine, the first spinal anesthetic, produces analgesia largely through its local anesthetic effect, but the noradrenergic stimulation of α2-receptors caused by its blocking of NE reuptake is also contributory. Therefore, '''it is the mimicking of the actions of descending inhibitory fibers by which clonidine, and all α2-agonists, causes analgesia'''. It has been shown that administration of the α2-antagonist, yohimbine, will at least partially reverse the sedation and analgesia induced by clonidine. [http://journals.lww.com/anesthesiology/Citation/1996/09000/Alpha_sub_2__Adrenergic_Agonists_for_Regional.26.aspx Eisenach J et al. Anesthesiology 85: 655, 1996 (FREE Full Text)]
 
This is only part of the story, however, as '''cholinergic activation in the dorsal horn has also been shown to impart analgesia, and clonidine has been shown to increase ACh levels in lumbar CSF'''. Additionally, '''epidural clonidine analgesia in volunteers is enhanced by intrathecal injection of the cholinesterase inhibitor, neostigmine''', lending further support to the notion that α2-agonists impart analgesia through both cholinergic and noradrenergic transmission. [http://journals.lww.com/anesthesiology/Citation/1996/09000/Alpha_sub_2__Adrenergic_Agonists_for_Regional.26.aspx Eisenach J et al. Anesthesiology 85: 655, 1996 (FREE Full Text)]
 
'''Clonidine also potentiates sensory and motor blockade of epidural and peripheral nerve block administered local anesthetics'''. Three mechanisms for this have been given. First, '''clonidine has intrinsic ability to block conduction in C and Aδ fibers''' and will intensify conduction block of local anesthetics. Second, '''clonidine may cause local vasoconstriction''' and thus impair vascular removal of epidural local anesthetics, although this probably does not occur significantly at clinically-used concentrations. '''Third, it has been shown that any analgesic, whether neuraxial or systemic, will augment peripheral or spinal blockade'''. Clonidine also enhances neuraxial opioids, with epidural clonidine and fentanyl interacting in an additive manner. In fact, the dose of each component can be reduced by 60% when combined for postoperative analgesia. [http://journals.lww.com/anesthesiology/Citation/1996/09000/Alpha_sub_2__Adrenergic_Agonists_for_Regional.26.aspx Eisenach J et al. Anesthesiology 85: 655, 1996 (FREE Full Text)]

[[Category: ABA Keywords]]

Evoked potentials: anesthetic effects

2010-09-06T18:48:01Z

New page: The purpose of intraoperative evoked potentials is to monitor neural pathways in hopes of avoiding iatrogenic injury to the nervous system. Sensory evoked potentials (SEPs) evaluate the i...

New page

The purpose of intraoperative evoked potentials is to monitor neural pathways in hopes of avoiding iatrogenic injury to the nervous system. Sensory evoked potentials (SEPs) evaluate the integrity of ascending sensory tracts while motor evoked potentials (MEPs) deal with the functionality of descending motor pathways.
 
'''SENSORY EVOKED POTENTIALS'''
 
Three SEP modalities are used clinically: somatosensory (SSEP), auditory (BAEP), and visual (VEP). The amplitude of these potentials is much smaller than that of the background EEG and must be extracted from the surrounding “noise” using signal averaging. Compromise of a neurologic pathway is evident with an increase in the latency and/or a decrease in the amplitude of EP waveforms. All anesthetics influence EP waveforms to some degree.
 
'''EPs of cortical origin (i.e. the cortical portion of SSEPs and VEPs) are considered more prone to modification by anesthetics than brainstem potentials''' (i.e. BAEPs and subcortical portions of SSEPs). '''It is imperative to maintain constant anesthetic drug levels during recording of EPs'''. Bolusing IV infusions or abrupt changes in MAC values of inhaled agents can be detrimental, particularly during critical portions of a procedure. When recording cortical EPs (SSEPs and VEPs) one should generally incorporate intravenous techniques as high concentrations of volatiles can completely eliminate cortical EPs. Nevertheless, all volatile anesthetics increase cortical latency and decrease cortical amplitude. However, desflurane and sevoflurane appear to be more forgiving with SSEPs than agents such as enflurane and isoflurane. For instance, desflurane at up to 1 MAC without nitrous oxide is compatible with cortical median nerve SSEP monitoring during scoliosis surgery. Use of nitrous oxide should probably be avoided during EP monitoring as it exhibits profound depressant effects on SSEPs and VEPs when combined with a volatile agent.
 
''SSEPs'': Pathway = Dorsal columns (UE)/lateral funiculus (LE). Electrical stimulation of mixed nerve, cortical short latency waveforms measured. '''Decreased amplitude of 50% + 10% prolongation in latency are significant'''. Signal averaged. Volatiles = dose dependent decrease in amplitude, increase in latency (< 1.0 MAC is ideal, not required)
 
Brainstem potentials are quite resilient with regard to anesthetics and are considered compatible with most anesthetic regimens.
 
Regarding IV agents, studies on thiopental have shown that even with doses far in excess of what is required to produce an isoelectric EEG, SSEP and BAEP waveforms are preserved even if there is a predictable increase in latency and decrease in amplitude. '''Propofol increases latency and decreases amplitude of cortical EPs''', but is considered an integral component of balanced intravenous neurosurgical anesthesia. '''Opioids produce minimal changes in SEP waveforms''', even in high doses. Because of this, they are recommended for use as infusions during EP monitoring. Both clonidine and dexmedetomidine decrease anesthetic requirements and have minimal effects on cortical EPs and are considered safe to use during monitoring. For practical purposes, ALL intravenous agents have negligible effect on cortical SSEP's, except for etomidate and ketamine, which can actually increase amplitude. Propofol, in concentrations sufficient to induce burst suppression, will abolish later cortical responses, but not the primary cortical responses (N20/P22 for median nerve, P40/N45 for tibial nerve), which are used for monitoring.
 
'''MOTOR EVOKED POTENTIALS'''
 
Transcranial electrical stimulation of the motor strip is a reliable method of producing intraoperative motor potentials that can be recorded from the spinal cord, peripheral nerve, or muscle. '''MEPs are exquisitely sensitive to anesthetics, especially inhalational agents'''. Volatiles, therefore, should be avoided during recording of myogenic MEPs. Benzodiazepines, barbiturates, and propofol all depress MEPs, however, adequate recordings can be obtained during propofol anesthesia by controlling serum levels and increasing stimuli rates. Muscle relaxants can affect the recorded EMG response by depressing myoneural transmission. However, adequate MEP recordings can be achieved as long as one or two twitches on TOF can be maintained.

[[Category: ABA Keywords]]

Type I statistical error: definition

2010-09-06T18:34:35Z

←Older revision		Revision as of 18:34, 6 September 2010
(One intermediate revision not shown.)
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-	~~Statistical Errors~~	+	When posing a question to be studied, the null hypothesis is the hypothesis that there is no difference between two populations. '''Wrongly rejecting the null hypothesis''', or stating that there is a statistically significant difference in the data when in fact there is not (false positive), '''is called type I error or alpha error'''. The probability of type I error depends on the level of significance assigned by the investigator and the existence or nonexistence of a difference between the two experimental conditions. The smaller the chosen alpha value, the smaller is the likelihood of making a type I error. A probability value (p-value) should be chosen before collecting data, and is most typically .05 in biomedical research. A p-value of .05 means that there is a 5% chance of making a type I error.
-		+
-	~~The goal is~~ to ~~determine accurately if~~ the ~~Null Hypothesis~~ ( ~~default state~~ of ~~nature~~) ~~can~~ be ~~rejected~~ in ~~favor~~ of ~~the Alternative Hypothesis~~.	+

	A '''type I error''', exists if the Null Hypothesis is incorrectly rejected. A False Alarm. False Positive. Positive pregnancy test on a non pregnant patient.		A '''type I error''', exists if the Null Hypothesis is incorrectly rejected. A False Alarm. False Positive. Positive pregnancy test on a non pregnant patient.

	A level of significance of 5%, or 1 in 20, is arbitrary set. 5% chance of making a type I error. If p is probability and p <0.05, there is 5% chance that an observed difference occurred because of chance.		A level of significance of 5%, or 1 in 20, is arbitrary set. 5% chance of making a type I error. If p is probability and p <0.05, there is 5% chance that an observed difference occurred because of chance.
		+
		+	Why not always set a very small alpha value? The consequence of setting a p-value of .01 versus .05 is that there is an increased risk of making a type II or beta error. This is a failure to reject the null hypothesis when it is in fact false. The smaller the p-value, the more likely one is to make a type II error. The power of a test is 1-beta. '''The probability of making a type II error depends on 4 factors'''. 1) size of alpha (as discussed) 2) variability within a population (more variability results in greater likelihood of type II error) 3) sample size (more subjects results in less chance of type II error) and 4) the magnitude of difference between the experimental conditions (smaller differences result in higher likelihood of type II error).
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		+	[[Category: ABA Keywords]]

Transcutaneous pacing

2010-09-06T18:29:24Z

New page

'''Indications:''' Hemodynamically significant (hypotension, chest pain, pulmonary edema, altered mental status) bradydysrhythmias unresponsive to atropine, asystolic cardiac arrest (more likely to be successful when initiated early after a witnessed arrest--unwitnessed arrest seldom responds to transcutaneous pacing), failed intrinsic pacemaker. When considering institution of transcutaneous pacing, always think about alternate causes for acute dysrhythmia, e.g. trauma, hypoxia, drug overdose, electrolyte imbalances and hypothermia. Treat underlying cause.

'''Technique:''' Ideal pacer pad placement “sandwiches” the heart between the pacing pads and mimics the heart’s normal electrical axis. Optimal placement for pads varies by manufacturer, but is generally anterior-posterior or anterior-lateral, with the former being most common. '''Begin at 10 milliamps and increase by increments of 10 until capture is noted'''. Target rate is generally 60-80 bpm. Strongly consider sedation, as external pacing can be quite uncomfortable. Most patients cannot tolerate currents of 50 milliamps and higher without sedation.

Mechanical capture of the ventricles is evidenced by signs of improved cardiac output, including a palpable pulse, rise in blood pressure, improved level of consciousness, improved skin color and temperature. Both electrical and mechanical capture must occur to benefit the patient.

'''It is safe to touch patients (e.g. to perform CPR) during pacing.'''

'''Pitfalls'''
 • Skeletal muscle contraction occurs at current levels as low as 10 milliamps, and does NOT suggest electrical or mechanical capture.
 • '''Most common reason for not obtaining capture is not adequately increasing the current'''. Current should be increased as much as necessary for electrical capture
 • Undersensing: when a pacemaker fails to detect intrinsic activity, and therefore delivers a pace pulse.
 • Oversensing is inappropriate inhibition of the pacemaker due to detection of signals other than R waves (e.g. muscle artifact).
 • Pacing thresholds may change without warning and capture can readily be lost.

[[Category: ABA Keywords]]

TPN: phosphorous deficiency

2010-09-06T18:23:36Z

←Older revision		Revision as of 18:23, 6 September 2010
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-	Refeeding syndrome results from ~~rapidly~~ changes in fluids and electrolytes when initiating nutrition in previously malnourished patients. It is primarily the result of hypophosphatemia ~~that results from a shift of fat to carbohydrate metabolism. Phosphorylated carbohydrate compounds form in the liver~~ and ~~muscle. ATP and 2,3-DPG are depleted, leading~~ to impaired myocardial contractility and cardiovascular collapse, as well as respiratory failure, rhabdomyolysis, seizures, ~~and~~ delirium.	+	'''Hypophosphatemia''' (defined as phosphate <2.5mg/dL) is '''reported in 17-28% of critically ill patients'''. It can result from increased renal excretion of phosphate, decreased absorption by the GI tract, or '''most commonly, an increase in intracellular movement of phosphate'''.
		+
		+	<br>'''Glucose loading, as occurs with administration of TPN, results in intracellular glucose movement'''. As TPN is instituted, glucose transport and oxidative phosphorylation acutely increase, resulting in increased demand for intracellular phosphate to support the formation of ATP. In patients with marginal extracellular phosphate levels, hypophosphatemia can rapidly develop. Hypophosphatemia may be responsible for the progressive weakness and inanition that characterizes “refeeding syndrome.”
		+
		+	<br>'''Refeeding syndrome''' results from rapid changes in fluids and electrolytes when initiating nutrition in previously malnourished patients. As mentioned above, patients who suffer from refeeding syndrome are usually ''hypophosphatemic'', as well as ''hypomagnesemic'' and ''hypokalemic''. TPN can exacerbate these conditions, especially secondary to glucose loading (leading to hypophosphatemia, as described above, as well as insulin release and worsened hypokalemia). It is primarily the result of hypophosphatemia and can lead to impaired myocardial contractility and cardiovascular collapse, as well as respiratory failure, rhabdomyolysis, seizures, delirium, and death.
		+
		+	<br>Risk of hypophosphatemia is one of the reasons why parenteral regimens are advanced slowly for the first few days. '''ALWAYS replete PO4, K, Mg prior to starting TPN'''

Special:Log/move

2010-09-06T17:11:20Z

TPN: phophorous deficiency moved to TPN: phosphorous deficiency: misspelling

Thyroidectomy: complications

2010-09-05T15:14:01Z

New page: Major postoperative complications include wound infection, bleeding, airway obstruction (compressing hematoma, tracheomalacia), hypocalcemia, thyroid storm (uncommon, usually associated wi...

New page

Major postoperative complications include wound infection, bleeding, airway obstruction (compressing hematoma, tracheomalacia), hypocalcemia, thyroid storm (uncommon, usually associated with Grave’s disease) and recurrent laryngeal nerve injury.

1) ''Wound infection''

Incidence is 0.2-0.5%.

2) ''Airway obstruction (compressing hematoma, trachiomalacia)''

Incidence of hematoma is 1-2%, Tracheomalacia incidence is <1%. Acute airway obstruction from hematoma may occur immediately postoperatively and is the most frequent cause of airway obstruction in the first 24 hours. Definitive therapy is opening the surgical incision to evacuate the hematoma. Re-intubation may be lifesaving for persistent airway obstruction. Consider awake fiberoptic intubation.

3) ''Recurrent laryngeal nerve injury''

Incidence of injury is '''0.77% for unilateral damage''' resulting in hoarseness and 0.39% for bilateral damage with associated aphonia and airway obstruction.

4) ''Hypocalcemia''

'''''Incidence is 3-5%'''''. Surgery can lead to trauma to the parathyroids, devascularization of the glands with resultant ischemia, or inadvertent excision of these small structures. Hypoparathyroidism with subsequent decreased production of parathyroid hormone leads to decreased serum calcium. '''Acute hypocalcemia generally presents at 24-48 hours as laryngeal stridor and airway obstruction'''. First symptoms are usually '''tingling in the lips and fingertips'''. Additional findings may develop, including carpopedal spasm, tetany, laryngospasm, seizures, QT prolongation and cardiac arrest. Chvostek’s sign is facial contractions elicited by tapping the facial nerve in the per-auricular area. Trouseau’s sign is carpal spasm on inflation of a blood pressure cuff. CPAP is often effective for associated airway compromise, and 1 gram of calcium gluconate given slowly usually alleviates symptoms.

'''*Airway obstruction: In the first 24 hours is most likely from compressive hematoma. After 24 hours consider laryngeal dysfunction secondary to hypocalcemia.'''

Succinylcholine: lower esophageal sphincter pressure

2010-09-03T15:09:28Z

←Older revision		Revision as of 15:09, 3 September 2010
Line 3:		Line 3:
	'''References''':		'''References''':

-	~~Cook~~, et Al. Lower Esophageal Sphincter Integrity Is Maintained During Succinylcholine-Induced Fasciaculations in Dogs With "Full" Stomachs Anesth Analg 1990; 70:420-423	+	<balloon title="During succinylcholine-induced muscle fasciculations, gas-troesophageal barrier pressure in fasted adult dogs (n = 10) was compared by esophageal manometry with that in the same dogs with full stomachs. After fasting, fasciculations did not increase significantly either mean intragastric pressure (4.7 ± 1.3 mm Hg before; 5.2 ± 1.7 mm Hg during) or lower esophageal sphincter pressure (35.4 ± 21.4 mm Hg before; 40.6 ± 17.5 mm Hg during). Filling the dogs' stomachs with 300 mL of saline significantly increased both mean intragastric pressure (from 3.8 ± 2.2 to 7.4 ± 1.4 mm Hg) and mean lower esophageal sphincter pressure (from 20.2 ± 6.8 to 28.6 ± 14.8 mm Hg). Fasciculations did not produce a further increase in either mean intragastric or mean lower esophageal sphincter pressure. Most importantly, in all animals, under all conditions, gastroesophageal barrier pressure remained positive (range, 6.0--65.5 mm Hg) and therefore served as a barrier to passive regurgitation" style="color:green">Cook WP et al. Lower Esophageal Sphincter Integrity Is Maintained During Succinylcholine-Induced Fasciaculations in Dogs With "Full" Stomachs Anesth Analg 1990; 70:420-423</balloon>

	Smith et al. GE Pressure Gradient changes produced by Anaesthesia and Suxamethonim, British Journal of Anaesthesia, 1978, Vol. 50, No. 11 1137-1143		Smith et al. GE Pressure Gradient changes produced by Anaesthesia and Suxamethonim, British Journal of Anaesthesia, 1978, Vol. 50, No. 11 1137-1143

QT prolongation with antiemetics

2010-09-03T15:07:16Z

Chu et. al.:

←Older revision		Revision as of 15:07, 3 September 2010
(2 intermediate revisions not shown.)
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	__TOC__		__TOC__
	=Review of Documented Cases: Habib et. al.=		=Review of Documented Cases: Habib et. al.=
-	The FDA warning is based on 10 reported cases from 1997-2002 [Habib et. al. ~~Anesthesia and Analgesia~~ 96: 1377, 2003] - these 10 cases were all with 1.25 mg or less, but in none of them could a definitive cause-effect relationship be described, and in five of them there were substantial confounding factors. Assuming that droperidol sales averaged 11 MM ampules per year, and that these events were truly related to droperidol, the authors estimated that the incidence of associated events was 1:150,000.	+	The FDA warning is based on 10 reported cases from 1997-2002 [Habib et. al. Anesth Analg 96: 1377, 2003; [http://www.anesthesia-analgesia.org/content/96/5/1377.full FREE Full-text at Anesthesia & Analgesia]] - these 10 cases were all with 1.25 mg or less, but in none of them could a definitive cause-effect relationship be described, and in five of them there were substantial confounding factors. Assuming that droperidol sales averaged 11 MM ampules per year, and that these events were truly related to droperidol, the authors estimated that the incidence of associated events was 1:150,000.

	=Smaller Studies=		=Smaller Studies=
Line 9:		Line 9:

	==Chu et. al.==		==Chu et. al.==
-	Another small study (400 total patients, randomized, prospective, controlled) studied haloperidol plus dexamethasone on PONV versus placebo and droperidol alone in vaginal hysterectomy patients. Haloperidol plus dexamethasone produced the greatest reduction in PONV when compared to placebo, either drug alone, or droperidol alone. There was no difference in QT prolongation in the haloperidol plus dexamethasone vs. droperidol alone {Chu et. al. Anesth Analg 106: 1402, 2008}	+	Another small study (400 total patients, randomized, prospective, controlled) studied haloperidol plus dexamethasone on PONV versus placebo and droperidol alone in vaginal hysterectomy patients. Haloperidol plus dexamethasone produced the greatest reduction in PONV when compared to placebo, either drug alone, or droperidol alone. There was no difference in QT prolongation in the haloperidol plus dexamethasone vs. droperidol alone [<balloon title="BACKGROUND: Haloperidol, a major tranquilizer, has been found to have a potent antiemetic effect on postoperative nausea and vomiting (PONV), but the prophylactic effect of haloperidol plus dexamethasone on PONV has not been evaluated. We evaluated the prophylactic effect of haloperidol plus dexamethasone to either given alone, placebo or droperidol on PONV in patients undergoing a laparoscopic-assisted vaginal hysterectomy.
		+	METHODS: Four hundred adult women (n = 80 in each of five groups) scheduled for a laparoscopic-assisted vaginal hysterectomy were enrolled in a randomized, double-blind, placebo, and positive-control study. Fifteen minutes after the induction of anesthesia, patients received an IV injection of either saline (group S), droperidol 1.25 mg (group D), haloperidol 2 mg (group H), dexamethasone 5 mg (group Dx), or haloperidol 2 mg plus dexamethasone 5 mg (group H + Dx) to prevent PONV. The occurrence of PONV and medication-related side effects were recorded.
		+	RESULTS: The incidences of PONV (0–24 h) in the D (36%), H (37%), Dx (38%), and H + Dx (19%) groups were significantly lower than in the S group (65%; P less than 0.05 for each comparison). The H + Dx group had the lowest incidence of PONV (19%; P less than 0.05 for each comparison) of the five study groups. No differences were found between the D, H, and Dx groups. Also, no differences were found among the five groups in the side effects of QT prolongation, intensity of postoperative pain, level of sedation, and occurrence of extra-pyramidal symptoms.
		+	CONCLUSION: Prophylactic haloperidol 2 mg plus dexamethasone 5 mg produced a greater reduction in the incidence of PONV than did either drug used alone, placebo or droperidol without increasing perioperative adverse outcomes. " style="color:green">Chu et. al. Anesth Analg 106: 1402, 2008</balloon>; [http://www.anesthesia-analgesia.org/content/106/5/1402.full FREE Full-text at Anesthesia & Analgesia]]

	==Nuttal et. al.==		==Nuttal et. al.==

Asthma (Concomitant Diseases)

2010-09-03T14:26:02Z

←Older revision		Revision as of 14:26, 3 September 2010
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	''Induction/Intubation:'' consider an '''LMA''' (less stimulating). Pre-induce with IV lidocaine (reduces airway reactivity). '''Propofol''' is the IV induction agent of choice, although '''ketamine''', which induces bronchodilation through neural mechanims and secondary to catecholamine release, should be considered in patients who are actively wheezing but have an urgent need for surgery and anesthesia. Propofol has been shown to produce less wheezing than thiopental and methohexital [<balloon title="BACKGROUND: Patients with asthma who require general anesthesia and tracheal intubation are at increased risk for the development of bronchospasm during induction. The incidence of wheezing during induction with different intravenously administered agents is unknown. A randomized, double-blinded prospective study was undertaken to evaluate the incidence of wheezing in asymptomatic asthmatic and nonasthmatic patients receiving three commonly used intravenous anesthetic agents for induction of anesthesia. METHODS: Fifty-nine asymptomatic asthmatic and 96 nonasthmatic patients of ASA physical status 1 and 2 were studied. All patients received 1.5 micrograms/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital or 2.5 mg/kg propofol, 1.5 mg/kg succinylcholine, tracheal intubation, and inhalational anesthesia. Wheezing was assessed by an independent blinded observer, auscultating the lungs at 2 and 5 min postintubation. Data were analyzed by Pearson's chi-squared, Fisher's exact test, and multiple logistic regression with significance set at P less than 0.05. RESULTS: Both asthmatic and nonasthmatic patients who received a thiobarbiturate for induction had a greater incidence of wheezing than did patients receiving propofol. In asthmatic patients, 45% (23, 67) (mean and 95% confidence interval) who received a thiobarbiturate, 26% (8, 44) who received an oxybarbiturate, and none (0, 17) who received propofol wheezed after intubation. In nonasthmatic patients, 16% (3, 28) who received thiobarbiturate and 3% (0, 9) who received propofol wheezed. CONCLUSIONS: This study suggests that propofol should be considered for induction of anesthesia in patients, particularly those with asthma, who require timely intubation." style="color:green">Pizov R et al. Anesthesiology 82: 1111, 1995</balloon>] and less respiratory resistance than thiopental and etomidate [<balloon title="BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate." style="color:green">Eames WO et al. Anesthesiology 84: 1307, 1996</balloon>]. Consider masking with an added volatile agent prior to direct laryngoscopy (deepens anesthesia, and sevoflurane is also a bronchodilator).		''Induction/Intubation:'' consider an '''LMA''' (less stimulating). Pre-induce with IV lidocaine (reduces airway reactivity). '''Propofol''' is the IV induction agent of choice, although '''ketamine''', which induces bronchodilation through neural mechanims and secondary to catecholamine release, should be considered in patients who are actively wheezing but have an urgent need for surgery and anesthesia. Propofol has been shown to produce less wheezing than thiopental and methohexital [<balloon title="BACKGROUND: Patients with asthma who require general anesthesia and tracheal intubation are at increased risk for the development of bronchospasm during induction. The incidence of wheezing during induction with different intravenously administered agents is unknown. A randomized, double-blinded prospective study was undertaken to evaluate the incidence of wheezing in asymptomatic asthmatic and nonasthmatic patients receiving three commonly used intravenous anesthetic agents for induction of anesthesia. METHODS: Fifty-nine asymptomatic asthmatic and 96 nonasthmatic patients of ASA physical status 1 and 2 were studied. All patients received 1.5 micrograms/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital or 2.5 mg/kg propofol, 1.5 mg/kg succinylcholine, tracheal intubation, and inhalational anesthesia. Wheezing was assessed by an independent blinded observer, auscultating the lungs at 2 and 5 min postintubation. Data were analyzed by Pearson's chi-squared, Fisher's exact test, and multiple logistic regression with significance set at P less than 0.05. RESULTS: Both asthmatic and nonasthmatic patients who received a thiobarbiturate for induction had a greater incidence of wheezing than did patients receiving propofol. In asthmatic patients, 45% (23, 67) (mean and 95% confidence interval) who received a thiobarbiturate, 26% (8, 44) who received an oxybarbiturate, and none (0, 17) who received propofol wheezed after intubation. In nonasthmatic patients, 16% (3, 28) who received thiobarbiturate and 3% (0, 9) who received propofol wheezed. CONCLUSIONS: This study suggests that propofol should be considered for induction of anesthesia in patients, particularly those with asthma, who require timely intubation." style="color:green">Pizov R et al. Anesthesiology 82: 1111, 1995</balloon>] and less respiratory resistance than thiopental and etomidate [<balloon title="BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate." style="color:green">Eames WO et al. Anesthesiology 84: 1307, 1996</balloon>]. Consider masking with an added volatile agent prior to direct laryngoscopy (deepens anesthesia, and sevoflurane is also a bronchodilator).

-	''Maintenance:'' sevoflurane (bronchodilator), although a propofol TIVA may also be reasonable. Use '''short-acting paralytics''' so as to avoid reversal (neostigmine can cause bronchoconstriction, and outlasts atropine). Consider an '''IV lidocaine infusion''' throughout the case, although lidocaine, which reduces airway responsiveness, has been shown to increase airway tone in asthmatic volunteers [<balloon title="BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, greater than 8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS: Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P less than 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION: Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration." style="color:green">Chang HY et al. Anesth Analg 104: 1109, 2007</balloon>]. Consider maintaining with 50% oxygen, as an FiO2 of 1.0 may abolish hypoxic pulmonary vasoconstriction. '''Beware steroid dependence''' (HPA axis assumed dysfunctional up to 1 year after IV steroids) and have access to IV agents. Beware breath-stacking, and '''consider shortening the I:E ratio'''	+	''Maintenance:'' sevoflurane (bronchodilator), although a propofol TIVA may also be reasonable. Use '''short-acting paralytics''' so as to avoid reversal (neostigmine can cause bronchoconstriction, and outlasts atropine). Consider an '''IV lidocaine infusion''' throughout the case, although lidocaine, which reduces airway responsiveness, has been shown to increase airway tone in asthmatic volunteers [<balloon title="BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, greater than 8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS: Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P less than 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION: Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration." style="color:green">Chang HY et al. Anesth Analg 104: 1109, 2007</balloon>; [http://www.anesthesia-analgesia.org/content/104/5/1109.full FREE Full-text at Anesthesia & Analgesia]]. Consider maintaining with 50% oxygen, as an FiO2 of 1.0 may abolish hypoxic pulmonary vasoconstriction. '''Beware steroid dependence''' (HPA axis assumed dysfunctional up to 1 year after IV steroids) and have access to IV agents. Beware breath-stacking, and '''consider shortening the I:E ratio'''

	The most common cause of an '''introperative bronchospastic attack''' is light anesthesia - treat by applying 100% FiO2 and immediately deepening anesthesia (consider IV ketamine or propofol, as inhaled agents may take time). Suction the airway (secretions can be stimulating) and ensure that the ETT has not moved too deep. If these fail, consider adding inhaled bronchodilators (more than two puffs are required in the midst of wheezing). As a last resort, call for an ICU ventilator (peak pressures up to 120 cm H2O)		The most common cause of an '''introperative bronchospastic attack''' is light anesthesia - treat by applying 100% FiO2 and immediately deepening anesthesia (consider IV ketamine or propofol, as inhaled agents may take time). Suction the airway (secretions can be stimulating) and ensure that the ETT has not moved too deep. If these fail, consider adding inhaled bronchodilators (more than two puffs are required in the midst of wheezing). As a last resort, call for an ICU ventilator (peak pressures up to 120 cm H2O)
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	Propofol versus thiopental and etomidate for IV induction in asthma [<balloon title="BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate." style="color:green">Eames WO et al. Anesthesiology 84: 1307, 1996</balloon>]		Propofol versus thiopental and etomidate for IV induction in asthma [<balloon title="BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate." style="color:green">Eames WO et al. Anesthesiology 84: 1307, 1996</balloon>]

-	Effect of IV lidocaine infusion on airway tone in asthmatics [<balloon title="BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, greater than 8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS: Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P less than 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION: Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration." style="color:green">Chang HY et al. Anesth Analg 104: 1109, 2007</balloon>]	+	Effect of IV lidocaine infusion on airway tone in asthmatics [<balloon title="BACKGROUND: To prevent reflex-induced bronchoconstriction in patients with asthma, local anesthetics are commonly administered by aerosol or IV as adjunct medication. Lidocaine attenuates responsiveness to a neurally active stimulus that increases tone, but there is scant information about the effect of lidocaine on baseline airway tone. Therefore we examined the effects of IV lidocaine on baseline airway tone in asthmatic subjects. METHODS: Small, medium, and large airways (2-5, 5-8, greater than 8 mm diameter) were analyzed by computed tomography in 15 asthmatic volunteers under baseline conditions and during infusion of lidocaine. Changes in luminal airway diameter and wall thickness from baseline to during lidocaine infusion, and the change in pulmonary function induced by lidocaine, were analyzed. RESULTS: Lidocaine caused a significant decrease in the forced expiratory volume in 1 s pulmonary function measure (7 +/- 2%, P = 0.006). There was also a small but significant decrease in the airway luminal diameter at total lung capacity during lidocaine infusion compared to baseline (-3 +/- 0.5%, P less than 0.001). Moreover, there was a significant correlation between the change in forced expiratory volume in 1 s and the change in airway luminal diameter at total lung capacity (r2 = 0.47, P = 0.01). CONCLUSION: Lidocaine, which reduces airway responsiveness to drugs that cause bronchospasm through sensory nerve activation, did not reduce baseline airway tone. Instead, even when administered IV, lidocaine significantly increased airway tone and caused airway narrowing. Therefore, while the administration of lidocaine can prevent intubation-induced bronchospasm, the airways should be constantly monitored by auscultation even during IV lidocaine administration." style="color:green">Chang HY et al. Anesth Analg 104: 1109, 2007</balloon>; [http://www.anesthesia-analgesia.org/content/104/5/1109.full FREE Full-text at Anesthesia & Analgesia]]

	[[Category: Concomitant Diseases]]		[[Category: Concomitant Diseases]]
	[[Category: Pulmonary System]]		[[Category: Pulmonary System]]

Transplant Surgery (Guide)

2010-09-03T14:23:01Z

Kidney Transplant:

←Older revision		Revision as of 14:23, 3 September 2010
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	'''Risk:''' intraoperative risk of MI is 2-3% [Jaffe RA and Samuels, SI. Anesthesiologist's Manual of Surgical Procedures, 4th ed. LWW: Baltimore, p. 681, 2009]. Note that overall, cardiac causes are responsible for 44.4% of deaths in patients with ESRD. 38% of transplant candidates have CAD, and the 12-month mortality is 44% in these patients (versus 5% in those without CAD). This forms the rationale for aggressive preoperative testing, although there is no data to support this practice, which is particularly worrisome given that it entails the use of contrast [de Lemos JA and Hillis LD. J Am Soc Nephrol 7: 2044, 1996]. Dobutamine stress echo (DSE) has a sensitivity of 52-75% and a specificity of 74-76% for CAD, and 20% of ESRD patients with a negative DSE will suffer cardiac death or MI within 2 years [<balloon title="Prophylactic coronary revascularization may reduce the risk for cardiac events in diabetic renal transplant candidates. No published data exist on the accuracy of dobutamine stress echocardiography (DSE) for the diagnosis of angiographically defined coronary artery disease (CAD) in renal transplant candidates. The purpose of this study is to examine the accuracy of DSE for the detection of CAD in high-risk renal transplant candidates compared with coronary angiography. Fifty renal transplant candidates with diabetic nephropathy (39 patients) or end-stage renal disease (ESRD) from other causes (11 patients) underwent prospectively performed DSE, followed by quantitative coronary angiography (QCA) and qualitative visual assessment of CAD severity. Twenty of 50 DSE tests were positive for inducible ischemia. Twenty-seven patients (54%) had a stenosis of 50% or greater by QCA, 12 patients (24%) had a stenosis of greater than 70% by QCA, and 16 patients (32%) had a stenosis greater than 75% by visual estimation. The sensitivity and specificity of DSE for CAD diagnosis were respectively 52% and 74% compared with QCA stenosis of 50% or greater, 75% and 71% compared with QCA stenosis greater than 70%, and 75% and 76% for stenosis greater than 75% by visual estimate. On long-term follow-up (22.5 +/- 10.1 months), 6 of 30 patients (20%) with negative DSE results and 11 of 20 patients (55%) with positive DSE results had a cardiac death, myocardial infarction (MI), or coronary revascularization. Six of 27 patients (22%) with a QCA stenosis of 50% or greater had a cardiac death or MI compared with none of the 23 patients (0%) with QCA stenosis less than 50% (P = 0.025). We conclude that DSE is a useful but imperfect screening test for angiographically defined CAD in renal transplant candidates" style="color:green">Herzog CA et al. Am J Kidney Dis 33: 1080, 1999</balloon>]		'''Risk:''' intraoperative risk of MI is 2-3% [Jaffe RA and Samuels, SI. Anesthesiologist's Manual of Surgical Procedures, 4th ed. LWW: Baltimore, p. 681, 2009]. Note that overall, cardiac causes are responsible for 44.4% of deaths in patients with ESRD. 38% of transplant candidates have CAD, and the 12-month mortality is 44% in these patients (versus 5% in those without CAD). This forms the rationale for aggressive preoperative testing, although there is no data to support this practice, which is particularly worrisome given that it entails the use of contrast [de Lemos JA and Hillis LD. J Am Soc Nephrol 7: 2044, 1996]. Dobutamine stress echo (DSE) has a sensitivity of 52-75% and a specificity of 74-76% for CAD, and 20% of ESRD patients with a negative DSE will suffer cardiac death or MI within 2 years [<balloon title="Prophylactic coronary revascularization may reduce the risk for cardiac events in diabetic renal transplant candidates. No published data exist on the accuracy of dobutamine stress echocardiography (DSE) for the diagnosis of angiographically defined coronary artery disease (CAD) in renal transplant candidates. The purpose of this study is to examine the accuracy of DSE for the detection of CAD in high-risk renal transplant candidates compared with coronary angiography. Fifty renal transplant candidates with diabetic nephropathy (39 patients) or end-stage renal disease (ESRD) from other causes (11 patients) underwent prospectively performed DSE, followed by quantitative coronary angiography (QCA) and qualitative visual assessment of CAD severity. Twenty of 50 DSE tests were positive for inducible ischemia. Twenty-seven patients (54%) had a stenosis of 50% or greater by QCA, 12 patients (24%) had a stenosis of greater than 70% by QCA, and 16 patients (32%) had a stenosis greater than 75% by visual estimation. The sensitivity and specificity of DSE for CAD diagnosis were respectively 52% and 74% compared with QCA stenosis of 50% or greater, 75% and 71% compared with QCA stenosis greater than 70%, and 75% and 76% for stenosis greater than 75% by visual estimate. On long-term follow-up (22.5 +/- 10.1 months), 6 of 30 patients (20%) with negative DSE results and 11 of 20 patients (55%) with positive DSE results had a cardiac death, myocardial infarction (MI), or coronary revascularization. Six of 27 patients (22%) with a QCA stenosis of 50% or greater had a cardiac death or MI compared with none of the 23 patients (0%) with QCA stenosis less than 50% (P = 0.025). We conclude that DSE is a useful but imperfect screening test for angiographically defined CAD in renal transplant candidates" style="color:green">Herzog CA et al. Am J Kidney Dis 33: 1080, 1999</balloon>]

-	'''Induction/Airway:''' succinylcholine is NOT contraindicated in chronic renal failure patients [<balloon title="(IN LIEU OF ABSTRACT): Case reports of SCh-induced hyperkalemia and cardiac arrests in various disease settings continue to appear in the literature. However, we did not find additional case reports and studies of SCh-induced hyperkalemia in patients with renal failure. This, and the clinical experience of investigators who have safely used SCh in a large number of patients with renal failure corroborate the above conclusions that SCh, with the exceptions noted above, can be used safely in such patients." style="color:green">Thapa S and Brull SJ. Anesth Analg 91: 237, 2000</balloon>]. Consider a RSI as many of these patients are diabetic and may have autonomic neuropathy	+	'''Induction/Airway:''' succinylcholine is NOT contraindicated in chronic renal failure patients [<balloon title="(IN LIEU OF ABSTRACT): Case reports of SCh-induced hyperkalemia and cardiac arrests in various disease settings continue to appear in the literature. However, we did not find additional case reports and studies of SCh-induced hyperkalemia in patients with renal failure. This, and the clinical experience of investigators who have safely used SCh in a large number of patients with renal failure corroborate the above conclusions that SCh, with the exceptions noted above, can be used safely in such patients." style="color:green">Thapa S and Brull SJ. Anesth Analg 91: 237, 2000</balloon>; [http://www.anesthesia-analgesia.org/content/91/1/237.full FREE Full-text at Anesthesia & Analgesia]]. Consider a RSI as many of these patients are diabetic and may have autonomic neuropathy

	'''Lines and Monitors:''' central venous catheter for antithymocyte preparation and in order to maintain CVP 10-15 mm Hg. Consider an arterial line, although kidney tranplants are relatively safe and some authors recommend only standard ASA monitors [<balloon title="Standard ASA monitors may be all that are needed for these cases. Severe cardiac arrhythmias are not common [Heino A, Orko R, Rosenberg PH: Anaesthesiological complications in renal transplantation: A retrospective study of 500 transplantations. Acta Anaesthesiol Scand 1986; 30:574-580]" style="color:green">Miller's Anesthesia, 6th ed. Chapter 56: Churchill Livingstone, 2004</balloon>]		'''Lines and Monitors:''' central venous catheter for antithymocyte preparation and in order to maintain CVP 10-15 mm Hg. Consider an arterial line, although kidney tranplants are relatively safe and some authors recommend only standard ASA monitors [<balloon title="Standard ASA monitors may be all that are needed for these cases. Severe cardiac arrhythmias are not common [Heino A, Orko R, Rosenberg PH: Anaesthesiological complications in renal transplantation: A retrospective study of 500 transplantations. Acta Anaesthesiol Scand 1986; 30:574-580]" style="color:green">Miller's Anesthesia, 6th ed. Chapter 56: Churchill Livingstone, 2004</balloon>]

On-Pump CABG (Guide)

2010-09-03T14:21:04Z

←Older revision		Revision as of 14:21, 3 September 2010
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	'''Risk:''' Mortality 2-4%; Morbidity: Congnitive decline post-op in Pts >60yo = 26%, CVA 2-4%, MI 3-6%. [Jaffe RA and Samuels, SI. Anesthesiologist's Manual of Surgical Procedures, 4th ed.]		'''Risk:''' Mortality 2-4%; Morbidity: Congnitive decline post-op in Pts >60yo = 26%, CVA 2-4%, MI 3-6%. [Jaffe RA and Samuels, SI. Anesthesiologist's Manual of Surgical Procedures, 4th ed.]

-	'''Induction:''' Appropriate induction of anesthesia for cardiac surgery is critical unique. By definition these patients have areas of myocardium that are at-risk or already ischemic. Traditional "Cardiac" induction consists of high dose narcotics, usually '''Fentanyl''' 10-100mcg/kg, '''Sufentanil''' 2-20mcg/kg, or '''Morphine''' 1-5mg/kg. Sufentanil has been associated with faster induction and recovery than Fentanyl or Morphine [<balloon title="ABSTRACT: We compared anesthetic doses of three popular opiates, morphine (n = 10), fentanyl (n = 9), and sufentanil (n = 9) in patients undergoing cardiac surgery. Opiate administration after induction was based upon EEG and cardiovascular signs of the depth of anesthesia. Total doses were morphine, 4.4 ± 0.71 mg/kg, fentanyl, 95.4 ± 9.9 µg/kg, and sufentanil, 18.9 ± 2.2 µg/kg. Comparisons among opiates included times for induction of anesthesia, return of consciousness, return of spontaneous ventilation, return of adequate cardiovascular status, and extubation. The following times (mean and SEM) were significantly shorter for sufentanil than for fentanyl or morphine: induction (15 ± 2.3 min, 5.9 ± 0.7 min, and 3.0 ± 0.2 min for morphine, fentanyl, and sufentanil, respectively); return of consciousness (morphine 109.7 ± 34.4 min, fentanyl 62.3 ± 17.9 min, sufentanil 77 ± 8.7 min); return of acceptable and stable cardiovascular status (morphine 587.3 ± 239.3 min, fentanyl 537.9 ± 144.8 min, sufentanil 173.7 ± 56.8 min); and extubation (morphine 1122.3 ± 61.8 min, fentanyl 1005.7 ± 77.7 min, sufentanil 533.3 ± 67.8 min). We conclude that sufentanil administered in the dosage range of 19 µg/kg allows more rapid induction, earlier emergence from anesthesia, and faster extubation of patients than either morphine or fentanyl" style="color:green">Sanford TJ Anesth Analg. 1986 Mar;65(3):259 PMID: 2937352</balloon>]. However, a recent study reported Morphine resulted in better quality of recovery and post-op pain control than Fentanyl [<balloon title="BACKGROUND: Experimental and clinical data suggest that morphine possesses unique cardioprotective and antiinflammatory properties. In this clinical investigation, we sought to determine whether the choice of intraoperative opioid (morphine or fentanyl) influences early recovery after cardiac surgery. METHODS: Ninety patients undergoing cardiac surgery with cardiopulmonary bypass were randomized to receive either morphine (40 mg) or fentanyl (600 µg) as part of a standardized opioid-isoflurane anesthetic. Quality of recovery was assessed using the QoR-40 questionnaire administered preoperatively and daily on postoperative days 1-3. During the first three postoperative days, pain was measured using a 100-mm visual analog scale, and the use of IV and oral pain medications (morphine or acetaminophen/hydrocodone) was quantified. Hemodynamic variables, duration of tracheal intubation, postoperative febrile reactions, organ morbidities, and intensive care unit (ICU) and hospital length of stay were evaluated. RESULTS: Compared with patients given fentanyl, those receiving morphine had higher global QoR-40 scores on postoperative days 1 (173 vs 160, P 0.0001), 2 (174 vs 164, P 0.0001), and 3 (177 vs 167, P 0.001). Differences between the groups were observed in the QoR-40 dimensions of emotional state, physical comfort, and pain (all P 0.01-0.0001). Postoperative visual analog scale pain scores, use of pain medication in the ICU and surgical ward, and postoperative febrile reactions were reduced significantly in the morphine group (all P 0.01). No differences between the groups were noted in duration of tracheal intubation, ICU and hospital length of stay, or postoperative complications. CONCLUSIONS: In patients undergoing elective cardiac surgery with cardiopulmonary bypass, postoperative quality-of-life measures and pain control during recovery were enhanced when morphine (40 mg) was administered intraoperatively as part of a balanced anesthetic technique compared with fentanyl" style="color:green">Murphy GS Anesth Analg 2009; 109:311</balloon>].	+	'''Induction:''' Appropriate induction of anesthesia for cardiac surgery is critical unique. By definition these patients have areas of myocardium that are at-risk or already ischemic. Traditional "Cardiac" induction consists of high dose narcotics, usually '''Fentanyl''' 10-100mcg/kg, '''Sufentanil''' 2-20mcg/kg, or '''Morphine''' 1-5mg/kg. Sufentanil has been associated with faster induction and recovery than Fentanyl or Morphine [<balloon title="ABSTRACT: We compared anesthetic doses of three popular opiates, morphine (n = 10), fentanyl (n = 9), and sufentanil (n = 9) in patients undergoing cardiac surgery. Opiate administration after induction was based upon EEG and cardiovascular signs of the depth of anesthesia. Total doses were morphine, 4.4 ± 0.71 mg/kg, fentanyl, 95.4 ± 9.9 µg/kg, and sufentanil, 18.9 ± 2.2 µg/kg. Comparisons among opiates included times for induction of anesthesia, return of consciousness, return of spontaneous ventilation, return of adequate cardiovascular status, and extubation. The following times (mean and SEM) were significantly shorter for sufentanil than for fentanyl or morphine: induction (15 ± 2.3 min, 5.9 ± 0.7 min, and 3.0 ± 0.2 min for morphine, fentanyl, and sufentanil, respectively); return of consciousness (morphine 109.7 ± 34.4 min, fentanyl 62.3 ± 17.9 min, sufentanil 77 ± 8.7 min); return of acceptable and stable cardiovascular status (morphine 587.3 ± 239.3 min, fentanyl 537.9 ± 144.8 min, sufentanil 173.7 ± 56.8 min); and extubation (morphine 1122.3 ± 61.8 min, fentanyl 1005.7 ± 77.7 min, sufentanil 533.3 ± 67.8 min). We conclude that sufentanil administered in the dosage range of 19 µg/kg allows more rapid induction, earlier emergence from anesthesia, and faster extubation of patients than either morphine or fentanyl" style="color:green">Sanford TJ Anesth Analg. 1986 Mar;65(3):259 PMID: 2937352</balloon>]. However, a recent study reported Morphine resulted in better quality of recovery and post-op pain control than Fentanyl [<balloon title="BACKGROUND: Experimental and clinical data suggest that morphine possesses unique cardioprotective and antiinflammatory properties. In this clinical investigation, we sought to determine whether the choice of intraoperative opioid (morphine or fentanyl) influences early recovery after cardiac surgery. METHODS: Ninety patients undergoing cardiac surgery with cardiopulmonary bypass were randomized to receive either morphine (40 mg) or fentanyl (600 µg) as part of a standardized opioid-isoflurane anesthetic. Quality of recovery was assessed using the QoR-40 questionnaire administered preoperatively and daily on postoperative days 1-3. During the first three postoperative days, pain was measured using a 100-mm visual analog scale, and the use of IV and oral pain medications (morphine or acetaminophen/hydrocodone) was quantified. Hemodynamic variables, duration of tracheal intubation, postoperative febrile reactions, organ morbidities, and intensive care unit (ICU) and hospital length of stay were evaluated. RESULTS: Compared with patients given fentanyl, those receiving morphine had higher global QoR-40 scores on postoperative days 1 (173 vs 160, P 0.0001), 2 (174 vs 164, P 0.0001), and 3 (177 vs 167, P 0.001). Differences between the groups were observed in the QoR-40 dimensions of emotional state, physical comfort, and pain (all P 0.01-0.0001). Postoperative visual analog scale pain scores, use of pain medication in the ICU and surgical ward, and postoperative febrile reactions were reduced significantly in the morphine group (all P 0.01). No differences between the groups were noted in duration of tracheal intubation, ICU and hospital length of stay, or postoperative complications. CONCLUSIONS: In patients undergoing elective cardiac surgery with cardiopulmonary bypass, postoperative quality-of-life measures and pain control during recovery were enhanced when morphine (40 mg) was administered intraoperatively as part of a balanced anesthetic technique compared with fentanyl" style="color:green">Murphy GS Anesth Analg 2009; 109:311</balloon>; [http://www.anesthesia-analgesia.org/content/109/2/311.full FREE Full-text at Anesthesia & Analgesia]].

	'''Lines and Monitors:''' Arterial line should be placed prior to induction. Right IJ MAC can be placed pre or post induction. Pulmonary Artery Catheter placement is common for nearly all cardiac surgeries. There is debate about whether PAC use is beneficial [<balloon title="BACKGROUND: Some observational studies suggest that the use of pulmonary-artery catheters to guide therapy is associated with increased mortality. METHODS: We performed a randomized trial comparing goal-directed therapy guided by a pulmonary-artery catheter with standard care without the use of a pulmonary-artery catheter. The subjects were high-risk patients 60 years of age or older, with American Society of Anesthesiologists (ASA) class III or IV risk, who were scheduled for urgent or elective major surgery, followed by a stay in an intensive care unit. Outcomes were adjudicated by observers who were unaware of the treatment-group assignments. The primary outcome was in-hospital mortality from any cause. RESULTS: Of 3803 eligible patients, 1994 (52.4 percent) underwent randomization. The base-line characteristics of the two treatment groups were similar. A total of 77 of 997 patients who underwent surgery without the use of a pulmonary-artery catheter (7.7 percent) died in the hospital, as compared with 78 of 997 patients in whom a pulmonary-artery catheter was used (7.8 percent)--a difference of 0.1 percentage point (95 percent confidence interval, -2.3 to 2.5). There was a higher rate of pulmonary embolism in the catheter group than in the standard-care group (8 events vs. 0 events, P=0.004). The survival rates at 6 months among patients in the standard-care and catheter groups were 88.1 and 87.4 percent, respectively (difference, -0.7 percentage point [95 percent confidence interval, -3.6 to 2.2]; negative survival differences favor standard care); at 12 months, the rates were 83.9 and 83.0 percent, respectively (difference, -0.9 percentage point [95 percent confidence interval, -4.3 to 2.4]). The median hospital stay was 10 days in each group. CONCLUSIONS: We found no benefit to therapy directed by pulmonary-artery catheter over standard care in elderly, high-risk surgical patients requiring intensive care" style="color:green">Sandham JD N Engl J Med 2003 Jan 2;348(1):5</balloon>]. However, many cardiac surgeons and anesthesiologist are accustomed to the information provided by the PAC and use this info to guide treatment intra-op and post-op.		'''Lines and Monitors:''' Arterial line should be placed prior to induction. Right IJ MAC can be placed pre or post induction. Pulmonary Artery Catheter placement is common for nearly all cardiac surgeries. There is debate about whether PAC use is beneficial [<balloon title="BACKGROUND: Some observational studies suggest that the use of pulmonary-artery catheters to guide therapy is associated with increased mortality. METHODS: We performed a randomized trial comparing goal-directed therapy guided by a pulmonary-artery catheter with standard care without the use of a pulmonary-artery catheter. The subjects were high-risk patients 60 years of age or older, with American Society of Anesthesiologists (ASA) class III or IV risk, who were scheduled for urgent or elective major surgery, followed by a stay in an intensive care unit. Outcomes were adjudicated by observers who were unaware of the treatment-group assignments. The primary outcome was in-hospital mortality from any cause. RESULTS: Of 3803 eligible patients, 1994 (52.4 percent) underwent randomization. The base-line characteristics of the two treatment groups were similar. A total of 77 of 997 patients who underwent surgery without the use of a pulmonary-artery catheter (7.7 percent) died in the hospital, as compared with 78 of 997 patients in whom a pulmonary-artery catheter was used (7.8 percent)--a difference of 0.1 percentage point (95 percent confidence interval, -2.3 to 2.5). There was a higher rate of pulmonary embolism in the catheter group than in the standard-care group (8 events vs. 0 events, P=0.004). The survival rates at 6 months among patients in the standard-care and catheter groups were 88.1 and 87.4 percent, respectively (difference, -0.7 percentage point [95 percent confidence interval, -3.6 to 2.2]; negative survival differences favor standard care); at 12 months, the rates were 83.9 and 83.0 percent, respectively (difference, -0.9 percentage point [95 percent confidence interval, -4.3 to 2.4]). The median hospital stay was 10 days in each group. CONCLUSIONS: We found no benefit to therapy directed by pulmonary-artery catheter over standard care in elderly, high-risk surgical patients requiring intensive care" style="color:green">Sandham JD N Engl J Med 2003 Jan 2;348(1):5</balloon>]. However, many cardiac surgeons and anesthesiologist are accustomed to the information provided by the PAC and use this info to guide treatment intra-op and post-op.
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	Results:Volatile anesthetics significantly enhanced diazoxide-mediated activation of mitoKATP channels as assessed by autofluorescence of myocytes. Conversely, volatile anesthetics alone did not alter mitoKATP channel activity, implying a priming effect of volatile anesthetics on mitoKATP channels. Administration of the protein kinase C inhibitor chelerythrine completely blocked this effect. Also, pretreatment with volatile anesthetics potentiated diazoxide-mediated protection against ischemia, as indicated by a reduction in trypan blue–positive myocytes. Importantly, cardioprotection afforded by volatile anesthetics was unaffected by the sarcKATP channel blocker HMR-1098 but sensitive to modulations of nitric oxide and adenosine–Gi signaling pathways.		Results:Volatile anesthetics significantly enhanced diazoxide-mediated activation of mitoKATP channels as assessed by autofluorescence of myocytes. Conversely, volatile anesthetics alone did not alter mitoKATP channel activity, implying a priming effect of volatile anesthetics on mitoKATP channels. Administration of the protein kinase C inhibitor chelerythrine completely blocked this effect. Also, pretreatment with volatile anesthetics potentiated diazoxide-mediated protection against ischemia, as indicated by a reduction in trypan blue–positive myocytes. Importantly, cardioprotection afforded by volatile anesthetics was unaffected by the sarcKATP channel blocker HMR-1098 but sensitive to modulations of nitric oxide and adenosine–Gi signaling pathways.
	Conclusions:Using autofluorescence in live cell imaging microscopy and a simulated model of ischemia, the authors present evidence that volatile anesthetics mediate their protection in cardiomyocytes by selectively priming mitoKATP channels through multiple triggering protein kinase C–coupled signaling pathways. These observations provide important new insight into the mechanisms of anesthetic-induced preconditioning." style="color:green">Zaugg M Anesthesiology 2002; 97:4-14</balloon>]. The most recent review article on this topic indicated that, although there is experimental and clinical data supporting cardioprotective effects of volatile anesthetics, there is still no evidence of an improvement in morbidity or mortality [<balloon title ="Conclusion: Well-designed animal studies have repeatedly demonstrated that exposure of the myocardium to a volatile anesthetic before a period of ischemia significantly protects the myocardium against subsequent ischemia-reperfusion injury. Similar to the protective effects of ischemic preconditioning, the anesthetic preconditioning effect is evidenced by better recovery of contractile function after ischemia and reduced infarct size in animal models.		Conclusions:Using autofluorescence in live cell imaging microscopy and a simulated model of ischemia, the authors present evidence that volatile anesthetics mediate their protection in cardiomyocytes by selectively priming mitoKATP channels through multiple triggering protein kinase C–coupled signaling pathways. These observations provide important new insight into the mechanisms of anesthetic-induced preconditioning." style="color:green">Zaugg M Anesthesiology 2002; 97:4-14</balloon>]. The most recent review article on this topic indicated that, although there is experimental and clinical data supporting cardioprotective effects of volatile anesthetics, there is still no evidence of an improvement in morbidity or mortality [<balloon title ="Conclusion: Well-designed animal studies have repeatedly demonstrated that exposure of the myocardium to a volatile anesthetic before a period of ischemia significantly protects the myocardium against subsequent ischemia-reperfusion injury. Similar to the protective effects of ischemic preconditioning, the anesthetic preconditioning effect is evidenced by better recovery of contractile function after ischemia and reduced infarct size in animal models.
-	The cardioprotective effect of volatile anesthetics has been supported by studies in patients during coronary surgery. However, further investigation is needed to determine whether the observed experimental and clinical cardioprotective effects of volatile anesthetics indeed translate into decreased morbidity and mortality in patients undergoing cardiac and noncardiac surgery" style="color:green">De Hert SG Anesth Analg 2005; 100:1584-1593</balloon>]. One interesting question to ask is, if current practice is to use Volatiles for cardiac surgery will an improvement in M & M change our practice? Likely not. However, the trend toward "fast-track" and even "ultra fast-track" cardiac surgery may eventually lead to a change in the standard use of volatile anesthetics in favor of TIVA. There is one recent study that compared Volatiles to TIVA for CABG. There was a difference in hospital length of stay (12 days for the TIVA group, 9 days for the SEVO group and 9 days for the DES group.) and 1 year mortality (12.3% in the TIVA group, 3.3% in the sevoflurane group, and 6.7% in the desflurane group), but the group assignment (TIVA, Sevo, Des) was not a significant independent predictor of 1 year mortality. [<balloon title="Summary: A randomised study of 414 patients undergoing coronary artery surgery with cardiopulmonary bypass was conducted to compare the effects of a volatile anaesthetic regimen with either deesflurane or sevoflurane, and a total intravenous anaesthesia (TIVA) regimen on postoperative troponin T release. The primary outcome variable was postoperative troponin T release, secondary outcome variables were hospital length of stay and 1-year mortality. Maximal postoperative troponin T values did not differ between groups (TIVA: 0.30 [0.00–4.79] ng.ml)1 (median [range]), sevoflurane: 0.33 [0.02–3.68] ng.ml)1, and desflurane: 0.39 [0.08–3.74] ng.ml)1). The independent predictors of hospital length of stay were the EuroSCORE (p 0.001), female gender (p = 0.042) and the group assignment (p 0.001). The one-year mortality was 12.3% in the TIVA group, 3.3% in the sevoflurane group, and 6.7% in the desflurane group. The EuroSCORE (p = 0.003) was the only significant independent predictor of 1-year mortality" style="color:green">De Hert SG Anaesthesia 2009; 64: p953–960</balloon>] Again, this only matters if we think TIVA is the future of anesthesia for cardiac surgery, which it may not be.	+	The cardioprotective effect of volatile anesthetics has been supported by studies in patients during coronary surgery. However, further investigation is needed to determine whether the observed experimental and clinical cardioprotective effects of volatile anesthetics indeed translate into decreased morbidity and mortality in patients undergoing cardiac and noncardiac surgery" style="color:green">De Hert SG Anesth Analg 2005; 100:1584-1593</balloon>; [http://www.anesthesia-analgesia.org/content/100/6/1584.full FREE Full-text at Anesthesia & Analgesia]]. One interesting question to ask is, if current practice is to use Volatiles for cardiac surgery will an improvement in M & M change our practice? Likely not. However, the trend toward "fast-track" and even "ultra fast-track" cardiac surgery may eventually lead to a change in the standard use of volatile anesthetics in favor of TIVA. There is one recent study that compared Volatiles to TIVA for CABG. There was a difference in hospital length of stay (12 days for the TIVA group, 9 days for the SEVO group and 9 days for the DES group.) and 1 year mortality (12.3% in the TIVA group, 3.3% in the sevoflurane group, and 6.7% in the desflurane group), but the group assignment (TIVA, Sevo, Des) was not a significant independent predictor of 1 year mortality. [<balloon title="Summary: A randomised study of 414 patients undergoing coronary artery surgery with cardiopulmonary bypass was conducted to compare the effects of a volatile anaesthetic regimen with either deesflurane or sevoflurane, and a total intravenous anaesthesia (TIVA) regimen on postoperative troponin T release. The primary outcome variable was postoperative troponin T release, secondary outcome variables were hospital length of stay and 1-year mortality. Maximal postoperative troponin T values did not differ between groups (TIVA: 0.30 [0.00–4.79] ng.ml)1 (median [range]), sevoflurane: 0.33 [0.02–3.68] ng.ml)1, and desflurane: 0.39 [0.08–3.74] ng.ml)1). The independent predictors of hospital length of stay were the EuroSCORE (p 0.001), female gender (p = 0.042) and the group assignment (p 0.001). The one-year mortality was 12.3% in the TIVA group, 3.3% in the sevoflurane group, and 6.7% in the desflurane group. The EuroSCORE (p = 0.003) was the only significant independent predictor of 1-year mortality" style="color:green">De Hert SG Anaesthesia 2009; 64: p953–960</balloon>] Again, this only matters if we think TIVA is the future of anesthesia for cardiac surgery, which it may not be.

Neuromuscular Blockade

2010-09-03T01:50:18Z

Benzylisoquinolones:

(Difference between revisions)

Subarachnoid Hemorrhage (Neuroanesthesia)

2010-09-02T23:54:47Z

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-	~~=SAH Anesthetic Considerations=~~
	[[Image:Subarachnoid_hemorrhage_CT.jpg\|thumb\|right\|200px\|CT of patient with a Subarachnoid Hemorrhage]]		[[Image:Subarachnoid_hemorrhage_CT.jpg\|thumb\|right\|200px\|CT of patient with a Subarachnoid Hemorrhage]]
		+	<br>
		+	=SAH Anesthetic Considerations=
	Anesthetic goals in this patient population revolve around 1) preventing large changes in blood pressure 2) facilitating surgical exposure [via hyperventilation and osmotic diuresis] 3) ensuring adequate collateral circulation if temporary clips are placed during surgery and 4) minimizing deleterious increases in ICP. As with other patients with CNS injury, remember to avoid hypoventilation (ie use opiates with caution)		Anesthetic goals in this patient population revolve around 1) preventing large changes in blood pressure 2) facilitating surgical exposure [via hyperventilation and osmotic diuresis] 3) ensuring adequate collateral circulation if temporary clips are placed during surgery and 4) minimizing deleterious increases in ICP. As with other patients with CNS injury, remember to avoid hypoventilation (ie use opiates with caution)

Special:Log/upload

2010-09-02T23:53:15Z

uploaded "Image:Subarachnoid hemorrhage CT.jpg"

Subarachnoid Hemorrhage (Neuroanesthesia)

2010-09-02T23:52:59Z

SAH Anesthetic Considerations:

←Older revision		Revision as of 23:52, 2 September 2010
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	=SAH Anesthetic Considerations=		=SAH Anesthetic Considerations=
		+	[[Image:Subarachnoid_hemorrhage_CT.jpg\|thumb\|right\|200px\|CT of patient with a Subarachnoid Hemorrhage]]
	Anesthetic goals in this patient population revolve around 1) preventing large changes in blood pressure 2) facilitating surgical exposure [via hyperventilation and osmotic diuresis] 3) ensuring adequate collateral circulation if temporary clips are placed during surgery and 4) minimizing deleterious increases in ICP. As with other patients with CNS injury, remember to avoid hypoventilation (ie use opiates with caution)		Anesthetic goals in this patient population revolve around 1) preventing large changes in blood pressure 2) facilitating surgical exposure [via hyperventilation and osmotic diuresis] 3) ensuring adequate collateral circulation if temporary clips are placed during surgery and 4) minimizing deleterious increases in ICP. As with other patients with CNS injury, remember to avoid hypoventilation (ie use opiates with caution)

Cardiac tamponade: Pulsus paradoxus

2010-09-02T19:49:35Z

New page: The pericardial sac typically has 15-30 ml fluid. Cardiac tamponade is caused by an increased amount of fluid in the pericardial sac, which compresses the heart. To a point, the body can ...

New page

The pericardial sac typically has 15-30 ml fluid. Cardiac tamponade is caused by an increased amount of fluid in the pericardial sac, which compresses the heart. To a point, the body can adapt by increased adrenergic tone which in turn increases systemic venous pressure and heart rate. This increase in pressure prevents the heart chambers from collapsing. And the increased heart rate preserves cardiac output despite decreased stroke volume.

At some point in the accumulation of fluid (around 250-300 ml), the pericardium reaches maximal distension and results in a phenomenon called pulsus paradoxus. Basically, the two ventricles are competing for space within the pericardial sac, so any increase in right ventricular volume (increased venous return during inspiration) results in the interatrial/ventricular septae to bulge leftwards. The opposite happens during expiration. This can be observed on the blood pressure waveform (defined by a drop in systolic blood pressure exceeding 10 mm Hg during inspiration), and on echocardiography.

Cardiac tamponade is the classic cause of pulsus paradoxus, but it can also be seen from a PE or hypovolemic shock. Many cardiac tamponade patients exhibit the classic "Beck Triad": low blood pressure, increased JVP, and distant heart sounds.

Anesthestic management for suspected cardiac tamponade could include arterial monitoring and CVP. Keep the heart "fast, full, and strong". Minimize positive pressure ventilation, especially high-volumes. And avoid drugs that cause myocardial depression or bradycardia.

Reference:
Miller's Anesthesia, 7th ed. Ch 60.

MAC Reduction

2010-09-02T19:29:09Z

MAC Reduction With Opiates: How To Use:

←Older revision		Revision as of 19:29, 2 September 2010
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	==MAC Reduction With Opiates: How To Use==		==MAC Reduction With Opiates: How To Use==
	===Concentration (ng/ml) Resulting in 50% MAC Reduction of Isoflurane===		===Concentration (ng/ml) Resulting in 50% MAC Reduction of Isoflurane===
-	<~~pre~~>	+	{\| style="border-collapse:collapse;text-align:center;" cellpadding="5" width="500"
-	Concentration (ng/ml) Resulting in 50% MAC Reduction of Isoflurane B) Calculated Potency	+	\|- style="border-top:2px solid #000;border-bottom:1px solid #000;"
-	Fentanyl 1.67 1x	+	\|align="left"\|
-	Sufentanil 0.14 12x	+	\|\|<b>Concentration (ng/ml)</b> <br> Resulting in 50% MAC Reduction of Isoflurane
-	Alfentanil 28.8* 1/16x (61/25)†	+	\|valign="top"\|<b>Calculated Potency</b>
-	Remifentanil 1.37‡ 1.2x	+	\|-
-	~~</pre>~~	+	\|align="left"\|Fentanyl \|\| 1.67 \|\| 1x
		+	\|-
		+	\|align="left"\|Sufentanil \|\| 0.14 \|\| 12x
		+	\|-
		+	\|align="left"\|Alfentanil \|\| 28.8* \|\| 1/16x (61/25)†
		+	\|- style="border-bottom:2px solid #000;"
		+	\|align="left"\|Remifentanil \|\| 1.37‡ \|\|1.2x
		+	\|}

-	~~===50% MAC Reduction of Isoflurane: IV Opiate Dosing ===~~
-	~~<pre>~~
-	~~Target Plasma Concentration (ng/ml) Bolus (ug/kg) Infusion Rate (ug/kg/min)~~
-	~~Fentanyl 1 3 0.020~~
-	~~Alfentanil 40 20 0.25~~
-	~~Sufentanil 0.15 0.15 0.003~~
-	~~Remifentanil 1 0.25 0.025~~

		+	===50% MAC Reduction of Isoflurane: IV Opiate Dosing ===
		+	{\| style="border-collapse:collapse; text-align:center;" cellpadding="5" width="500"
		+	\|- style="border-top:2px solid #000;border-bottom:1px solid #000;"
		+	\|align="left"\|
		+	\|\|<b>Target Plasma <br>Concentration </b>(ng/ml)
		+	\| valign="top"\|<b>Bolus <br>(ug/kg)</b>
		+	\| valign="top"\|<b>Infusion Rate<br> (ug/kg/min)</b>
		+	\|-
		+	\|align="left"\|Fentanyl \|\| 1 \|\| 3 \|\| 0.020
		+	\|-
		+	\|align="left"\|Alfentanil \|\| 40 \|\|20 \|\| 0.25
		+	\|-
		+	\|align="left"\|Sufentanil \|\| 0.15 \|\|0.15\|\|0.003
		+	\|-style="border-bottom:2px solid #000;"
		+	\|align="left"\|Remifentanil \|\| 1 \|\| 0.25\|\|0.025
		+	\|}
	*Remifentanil and alfentanil bolus should given as a rapid infusion over 1–2 minutes.		*Remifentanil and alfentanil bolus should given as a rapid infusion over 1–2 minutes.
-	~~</pre>~~

-	~~===Maximal MAC Reduction of Isoflurane: IV Opiate Dosing ===~~
-	~~<pre>~~
-	~~Target Plasma Concentration (ng/ml) Bolus (ug/kg) Infusion Rate (u/kg/min)~~
-	~~Fentanyl 4 10 0.070~~
-	~~Alfentanil 160 80* 1.00~~
-	~~Sufentanil 0.50 0.50 0.010~~
-	~~Remifentanil 5–15 1* 0.2–1.0~~

-	*Remifentanil and alfentanil bolus should given as a rapid infusion over 1–2 minutes.	+
-	~~</pre>~~	+	===Maximal MAC Reduction of Isoflurane: IV Opiate Dosing ===
		+	{\| style="border-collapse:collapse; text-align:center;" cellpadding="5" width="500"
		+	\|- style="border-top:2px solid #000;border-bottom:1px solid #000;"
		+	\|\|
		+	\|<b>Target Plasma <br>Concentration</b> (ng/ml)
		+	\|<b>Bolus </b><br>(ug/kg)
		+	\|<b>Infusion Rate</b> <br> (u/kg/min)
		+	\|-
		+	\|align="left"\|Fentanyl \|\| 4 \|\| 10 \|\| 0.070
		+	\|-
		+	\|align="left"\|Alfentanil \|\| 160 \|\| 80* \|\| 1.00
		+	\|-
		+	\|align="left"\|Sufentanil \|\| 0.50 \|\| 0.50 \|\|0.010
		+	\|- style="border-bottom:2px solid #000;"
		+	\|align="left"\|Remifentanil \|\| 5–15 \|\| 1* \|\| 0.2–1.0
		+	\|}
		+	*Remifentanil and alfentanil bolus should given as a rapid infusion over 1–2 minutes.

	==Concerns re: MAC Reduction: Opiate Sensitization==		==Concerns re: MAC Reduction: Opiate Sensitization==

User:Cp24

2010-09-02T19:10:45Z

←Older revision		Revision as of 19:10, 2 September 2010
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	this is a test page for my self.		this is a test page for my self.
	{{channing}}		{{channing}}
		+
		+	{\| style="border-collapse:collapse;" cellpadding="5"
		+	\|- style="border-top:2px solid #000;border-bottom:1px solid #000;"
		+	!align="left"\|
		+	\|-
		+	\|- style="border-bottom:2px solid #000;"
		+	\|}

Inhaled Anesthetics

2010-09-02T18:56:54Z

Neurologic System:

←Older revision		Revision as of 18:56, 2 September 2010
(4 intermediate revisions not shown.)
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	Point at which 50% of patients will not respond to a surgical incision. STD of MAC is 10%, thus 95% of patients will not respond to 1.2 MAC, and 99% will not respond to 1.3 MAC. According to rat data, MAC values are additive in terms of preventing movement to incision (0.5 MAC of nitrous oxide plus 0.5 MAC of isoflurane = 1.0 MAC of any other agent) [Rampill Anesthesiology 80: 606, 1994]		Point at which 50% of patients will not respond to a surgical incision. STD of MAC is 10%, thus 95% of patients will not respond to 1.2 MAC, and 99% will not respond to 1.3 MAC. According to rat data, MAC values are additive in terms of preventing movement to incision (0.5 MAC of nitrous oxide plus 0.5 MAC of isoflurane = 1.0 MAC of any other agent) [Rampill Anesthesiology 80: 606, 1994]

-	~~<pre>~~	+	{\| style="border-collapse:collapse;" cellpadding=5
-	Factors which Increase Anesthetic Requirements	+	\|- style="border-top:2px solid #000; border-bottom:1px solid #000;"
-	- Chronic ETOH	+	!style="background-color:#ffefef;"\|Factors which Increase Anesthetic Requirements
-	- Infant (highest MAC at 6 mo.)	+	!style="background-color:#efefff;"\|Factors which Decrease Anesthetic Requirements
-	- Red hair	+	\|- style="border-bottom:2px solid #000;"
-	- Hypernatremia	+	\|style="vertical-align:top;background-color:#ffefef"\|
-	- Hyperthermia	+	* Chronic ETOH
-		+	* Infant (highest MAC at 6 mo.)
-	~~Factors which Decrease Anesthetic Requirements~~	+	* Red hair
-	- Acute ETOH	+	* Hypernatremia
-	- Elderly Patients	+	* Hyperthermia
-	- Hyponatremia	+	\| style="vertical-align:top;background-color:#efefff"\|
-	- Hypothermia	+	* Acute ETOH
-	- Anemia (Hgb < 5 g/dL)	+	* Elderly Patients
-	- Hypercarbia	+	* Hyponatremia
-	- Hypoxia	+	* Hypothermia
-	- Pregnancy	+	* Anemia (Hgb < 5 g/dL)
-	~~</pre>~~	+	* Hypercarbia
		+	* Hypoxia
		+	* Pregnancy
		+	\|}

	==Pharmacokinetics==		==Pharmacokinetics==
Line 39:		Line 42:
	Complete equilibration with any tissue takes 3 time constants - time constant for isoflurane is 3-4 minutes, for sevoflurane, desflurane, or nitrous oxide is ~ 2 minutes. For all inhaled anesthetics, PI should therefore be decreased after 6-12 minutes		Complete equilibration with any tissue takes 3 time constants - time constant for isoflurane is 3-4 minutes, for sevoflurane, desflurane, or nitrous oxide is ~ 2 minutes. For all inhaled anesthetics, PI should therefore be decreased after 6-12 minutes

-	~~<pre>~~	+	{\| style="border-collapse:collapse; text-align:left;" cellpadding="5"
-	Time Constants and Brain Equilibration	+	\|+'''Time Constants and Brain Equilibration'''
-	Time constant Brain Equilibration time	+	\|- style = "border-top:2px solid #000; border-bottom:1px solid #000;"
-	Isoflurane 3-4 mins 10-15 mins	+	!align="left"\|
-	Sevoflurane 2 mins 6 mins	+	!align="left"\| Time constant
-	Desflurane 2 mins 6 mins	+	!align="left"\| Brain Equilibration time
-	Nitrous Oxide 2 mins 6 mins	+	\|-
-	~~</pre>~~	+	\|Isoflurane \|\| 3-4 mins \|\| 10-15 mins
		+	\|-
		+	\|Sevoflurane \|\| 2 mins \|\| 6 mins
		+	\|-
		+	\|Desflurane \|\| 2 mins \|\| 6 mins
		+	\|- style = "border-bottom:2px solid #000;"
		+	\|Nitrous Oxide \|\| 2 mins \|\| 6 mins
		+	\|}

	===Elimination and Recovery===		===Elimination and Recovery===
Line 54:		Line 64:
	===Circulatory System===		===Circulatory System===
	Inhaled anesthetics all cause a dose-dependent decrease in MAP due to decreases in SVR – this can be minimized by combining them with nitrous oxide [<balloon title="The length of anesthetic administration influences the rate at which concentrations of anesthetics decrease after their discontinuation. This is true for both intravenous (I.V.) and inhaled anesthetics. This has been explored in detail for I.V. anesthetics using computer simulation to calculate context-sensitive half-times (the time needed for a 50% decrease in anesthetic concentration) and other decrement times (such as the times needed for 80% or 90% decreases in anesthetic concentration). However, decrement times have not been reported for inhaled anesthetics. In this report, published pharmacokinetic parameters and computer simulation were used to compare the context-sensitive half-times and the 80% and 90% decrement times of the expected central nervous system concentrations for enflurane, isoflurane, sevoflurane, and desflurane. The context-sensitive half-times for all four anesthetics are small (less than 5 min) and do not increase significantly with increasing duration of anesthesia. The 80% decrement times of both sevoflurane and desflurane are also small (less than 8 min) and do not increase significantly with duration of anesthesia. However, the 80% decrement times of isoflurane and enflurane increase significantly after approximately 60 min of anesthesia, reaching plateaus of approximately 30 and 35 min. The 90% decrement time of desflurane increased slightly from 5 min after 30 min of anesthesia to 14 min after 6 h of anesthesia. It remained significantly less than the 90% decrement times of sevoflurane, isoflurane, and enflurane, which reached values of 65 min, 86 min, and 100 min, respectively, after 6 h of anesthesia. IMPLICATIONS: The major differences in the rates at which desflurane, sevoflurane, isoflurane, and enflurane are eliminated occur in the final 20% of the elimination process. " style="color:green">Bailey Anesth Analg 85: 681, 1997</balloon>], which has been shown to sometimes increase MAP. Inhaled anesthetics also cause increases in heart rate, although at different doses – sevoflurane is unique in that it does not appreciably increase HR until 1.5 MAC is achieved. Desflurane can actually stimulate the cardiovascular system, although this ability wanes as anesthesia is maintained. Sevoflurane, desflurane, and isoflurane all diminish baroreceptor responses. Because changes in MAP are due to SNS induced changes in SVR (and not cardiac stimulation or lack thereof), neither sevoflurane, desflurane, or isoflurane appreciably affect cardiac output in healthy volunteers [Cahalan Review Course IARS 1996: 14, 1996] – sevoflurane exhibits the most profound drop, from 100 L/min to 80 L/min as MAC goes from 0.0 to 1.0, however this increases back to 90 L/min as MAC approaches 2.0.		Inhaled anesthetics all cause a dose-dependent decrease in MAP due to decreases in SVR – this can be minimized by combining them with nitrous oxide [<balloon title="The length of anesthetic administration influences the rate at which concentrations of anesthetics decrease after their discontinuation. This is true for both intravenous (I.V.) and inhaled anesthetics. This has been explored in detail for I.V. anesthetics using computer simulation to calculate context-sensitive half-times (the time needed for a 50% decrease in anesthetic concentration) and other decrement times (such as the times needed for 80% or 90% decreases in anesthetic concentration). However, decrement times have not been reported for inhaled anesthetics. In this report, published pharmacokinetic parameters and computer simulation were used to compare the context-sensitive half-times and the 80% and 90% decrement times of the expected central nervous system concentrations for enflurane, isoflurane, sevoflurane, and desflurane. The context-sensitive half-times for all four anesthetics are small (less than 5 min) and do not increase significantly with increasing duration of anesthesia. The 80% decrement times of both sevoflurane and desflurane are also small (less than 8 min) and do not increase significantly with duration of anesthesia. However, the 80% decrement times of isoflurane and enflurane increase significantly after approximately 60 min of anesthesia, reaching plateaus of approximately 30 and 35 min. The 90% decrement time of desflurane increased slightly from 5 min after 30 min of anesthesia to 14 min after 6 h of anesthesia. It remained significantly less than the 90% decrement times of sevoflurane, isoflurane, and enflurane, which reached values of 65 min, 86 min, and 100 min, respectively, after 6 h of anesthesia. IMPLICATIONS: The major differences in the rates at which desflurane, sevoflurane, isoflurane, and enflurane are eliminated occur in the final 20% of the elimination process. " style="color:green">Bailey Anesth Analg 85: 681, 1997</balloon>], which has been shown to sometimes increase MAP. Inhaled anesthetics also cause increases in heart rate, although at different doses – sevoflurane is unique in that it does not appreciably increase HR until 1.5 MAC is achieved. Desflurane can actually stimulate the cardiovascular system, although this ability wanes as anesthesia is maintained. Sevoflurane, desflurane, and isoflurane all diminish baroreceptor responses. Because changes in MAP are due to SNS induced changes in SVR (and not cardiac stimulation or lack thereof), neither sevoflurane, desflurane, or isoflurane appreciably affect cardiac output in healthy volunteers [Cahalan Review Course IARS 1996: 14, 1996] – sevoflurane exhibits the most profound drop, from 100 L/min to 80 L/min as MAC goes from 0.0 to 1.0, however this increases back to 90 L/min as MAC approaches 2.0.
		+	<div style="float:left; margin:20px;">
		+	{\| style="border-collapse:collapse; text-align:left;" cellpadding="5" width="200"
		+	\|+MAC at which heart rate increases
		+	\|- style = "border-top:2px solid #000; border-bottom:1px solid #000;"
		+	!align="left"\|
		+	!align="left"\|MAC
		+	\|-
		+	\|Sevo \|\|1.5
		+	\|-
		+	\|Des \|\| 1.0
		+	\|- style = "border-bottom:2px solid #000;"
		+	\|Iso \|\|0.25

-	~~<pre>~~	+	\|}
-	~~MAC at which heart rate increases~~	+	</div>
-	~~MAC~~	+
-	~~Sevo 1.5~~	+
-	~~Des 1.0~~	+
-	~~Iso 0.25~~	+
-	</~~pre~~>	+
-		+
	Note that sudden changes in anesthetic concentration can elicit more profound cardiovascular effects. Sudden increase in desflurane from 4 to 8% can double heart rate and blood pressure (this can be attenuated with small doses of opioids, clonidine, or esmolol). This does not happen with sevoflurane [Ebert Anesthesiology 83: 88, 1995]		Note that sudden changes in anesthetic concentration can elicit more profound cardiovascular effects. Sudden increase in desflurane from 4 to 8% can double heart rate and blood pressure (this can be attenuated with small doses of opioids, clonidine, or esmolol). This does not happen with sevoflurane [Ebert Anesthesiology 83: 88, 1995]
	Sevoflurane, desflurane, and isoflurane do not predispose the heart to ventricular dysrhythmias [Navarro Anesthesiology 80: 545, 1994], and evidence from animal studies suggests that they may even suppress dysrhythmias related to ischemia [Miller]		Sevoflurane, desflurane, and isoflurane do not predispose the heart to ventricular dysrhythmias [Navarro Anesthesiology 80: 545, 1994], and evidence from animal studies suggests that they may even suppress dysrhythmias related to ischemia [Miller]
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	Nitrous oxide causes cerebral vasodilation and increases CBF in the absence of volatile anesthetics. Additionally, CMRO2 is mildly increased, however coadministration of opiates, barbiturates, or propfol (but not ketamine) attenuates these effects [Petersen Anesthesiology 98: 329, 2003]		Nitrous oxide causes cerebral vasodilation and increases CBF in the absence of volatile anesthetics. Additionally, CMRO2 is mildly increased, however coadministration of opiates, barbiturates, or propfol (but not ketamine) attenuates these effects [Petersen Anesthesiology 98: 329, 2003]
	Sevoflurane, desflurane, and isoflurane decrease CMRO2. They all vasodilate above 0.6 MAC and produce a biphasic effect on cerebral blood flow – at 0.5 MAC, CMRO2 decreases, and counteracts the vasodilatory effects (ie CBF does not change); above 1.0 MAC, vasodilatory effects become more prominent, and actually increase CBF		Sevoflurane, desflurane, and isoflurane decrease CMRO2. They all vasodilate above 0.6 MAC and produce a biphasic effect on cerebral blood flow – at 0.5 MAC, CMRO2 decreases, and counteracts the vasodilatory effects (ie CBF does not change); above 1.0 MAC, vasodilatory effects become more prominent, and actually increase CBF
-		+	{\| style="border-collapse:collapse; text-align:left;" cellpadding="5" width="500"
-	~~<pre>~~	+	\|+'''CNS Effects of Anesthetics'''
-	CNS Effects of Anesthetics	+	\|- style = "border-top:2px solid #000; border-bottom:1px solid #000;"
-	Tone CMRO2 CBF ICP	+	!align="left" width="100"\|
-	NO vasodil ~~incr incr~~	+	!align="left" width="100"\|Tone
-	Sevo vasodil decr incr* ~~incr~~*	+	!align="left" width="100"\|CMRO2
-	Des vasodil ~~decr incr~~* ~~incr~~*	+	!align="left" width="100"\|CBF
-	Iso vasodil decr incr* ~~incr~~*	+	!align="left" width="100"\| ICP
-		+	\|-
-	*because of CMRO2, CBF and ICP do not increase until MAC 1.0	+	\|NO \|\| vasodil \|\| ↑ \|\| ↑
-	~~</pre>~~	+	\|-
		+	\|Sevo \|\| vasodil \|\| ↓ \|\| ↑ * \|\| ↑ *
		+	\|-
		+	\|Des \|\| vasodil \|\| ↓ \|\| ↑ * \|\| ↑ *
		+	\|- style = "border-bottom:2px solid #000;"
		+	\|Iso \|\| vasodil \|\| ↓ \|\| ↑ * \|\| ↑ *
		+	\|}
		+	*because of CMRO2, CBF and ICP do not increase until MAC 1.0

	ICP increases for all inhaled agents at MAC 1.0, and autoregulation is impaired at levels below that. 1.0 MAC of isoflurane or desflurane decreases CBF during craniotomy for supratentorial tumors [Fraga Anesthesiology 98: 1085, 2003] but does not affect ICP. In contrast, 1.0 MAC of iso/des will decrease CBF and raise ICP in pituitary resections, and subjective measures of brain relaxation suggest that 50% NO plus 0.5 MAC of iso/des provide better relaxation [Miller]		ICP increases for all inhaled agents at MAC 1.0, and autoregulation is impaired at levels below that. 1.0 MAC of isoflurane or desflurane decreases CBF during craniotomy for supratentorial tumors [Fraga Anesthesiology 98: 1085, 2003] but does not affect ICP. In contrast, 1.0 MAC of iso/des will decrease CBF and raise ICP in pituitary resections, and subjective measures of brain relaxation suggest that 50% NO plus 0.5 MAC of iso/des provide better relaxation [Miller]

Category:ABA Keywords

2010-09-02T18:37:18Z

←Older revision		Revision as of 18:37, 2 September 2010
Line 1:		Line 1:
-	Below are the key words and phrases from the 2008 ~~and 2009~~ ABA inservice training (ITE) exams, followed by the percent of residents in their final year of training who answered the question pertaining to the key word correctly. Some (and soon, hopefully all) of these key words and phrases are discussed in detail on this site - click on the links to read more:	+	Below are the key words and phrases from the 2008 through 2010 ABA inservice training (ITE) exams, followed by the percent of residents in their final year of training who answered the question pertaining to the key word correctly. Some (and soon, hopefully all) of these key words and phrases are discussed in detail on this site - click on the links to read more:

	'''(note: please see our policy on [[Policy on Evidence Based Medicine]] and help us make these answers more robust by adding appropriate citations)'''		'''(note: please see our policy on [[Policy on Evidence Based Medicine]] and help us make these answers more robust by adding appropriate citations)'''

Special:Log/delete

2010-09-02T16:46:07Z

deleted "Floxin - floxin generic buy - floxin 400mg price": Vandalism: content was: ' <center><h1>[http://natoli.ru/pt/index.php?k=floxin&said=wiki CLICK HERE TO ENTER DRUGSTORE!]</h1> <h2>[http://natoli.ru/pt/index.p...' (and the only

Special:Log/block

2010-09-02T16:45:56Z

blocked User:Arilbine89pnkv with an expiry time of infinite (account creation disabled): Spamming links to external sites

Opioid Induced Hyperalgesia (Controversies)

2010-09-02T14:46:02Z

←Older revision		Revision as of 14:46, 2 September 2010
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	A study of 20 patients undergoing off-pump CABG with standard propofol/fentanyl anesthesia randomized them to receive either remifentanil at 0.1 ucg/kg/min versus placebo. At one hour post-operatively, the remifentanil group required 8.39 mg morphine, as compared to 3.29 mg in the placebo group (p < 0.01), however this difference resolved by 12 hours [<balloon title="BACKGROUND: We have prospectively assessed the effects of remifentanil on morphine requirement in the first hour after emerging from general anaesthesia after elective coronary artery bypass surgery and in the first 12 h postoperatively, and pain and agitation scores in the first hour after emerging from general anaesthesia. METHODS: Twenty patients undergoing off-pump coronary artery bypass surgery, receiving standardized propofol-fentanyl-based anaesthesia, randomly received infusions of either remifentanil 0.1 microg kg(-1) min(-1) (Group R, n=10) or saline (Group S, n=10), each infused at 0.12 ml kg(-1) h(-1). Propofol and trial drug infusion were continued into the postoperative period until the patients were ready to be woken up. Postoperative analgesia was provided with morphine infusion commenced immediately after operation, and was additionally nurse controlled on the basis of a visual analogue scale (VAS) score (0-10). Agitation score was recorded using a VAS of 0-3. RESULTS: In the first hour after discontinuing propofol and trial infusion, morphine requirements were significantly higher in the remifentanil group (8.15 (sd 3.59) mg) compared with the saline group (3.29 (2.36) mg) (P less than 0.01). There was no difference in the total morphine given during the period after stopping propofol or in the total requirement in the first 12 h postoperatively. There was no significant difference in either pain scores or agitation scores between the two groups. CONCLUSION: Use of remifentanil is associated with increased opioid requirement in the first hour after it has been discontinued." style="color:green">Rauf K et. al. Br J Anaesth 95: 611, 2005</balloon>]		A study of 20 patients undergoing off-pump CABG with standard propofol/fentanyl anesthesia randomized them to receive either remifentanil at 0.1 ucg/kg/min versus placebo. At one hour post-operatively, the remifentanil group required 8.39 mg morphine, as compared to 3.29 mg in the placebo group (p < 0.01), however this difference resolved by 12 hours [<balloon title="BACKGROUND: We have prospectively assessed the effects of remifentanil on morphine requirement in the first hour after emerging from general anaesthesia after elective coronary artery bypass surgery and in the first 12 h postoperatively, and pain and agitation scores in the first hour after emerging from general anaesthesia. METHODS: Twenty patients undergoing off-pump coronary artery bypass surgery, receiving standardized propofol-fentanyl-based anaesthesia, randomly received infusions of either remifentanil 0.1 microg kg(-1) min(-1) (Group R, n=10) or saline (Group S, n=10), each infused at 0.12 ml kg(-1) h(-1). Propofol and trial drug infusion were continued into the postoperative period until the patients were ready to be woken up. Postoperative analgesia was provided with morphine infusion commenced immediately after operation, and was additionally nurse controlled on the basis of a visual analogue scale (VAS) score (0-10). Agitation score was recorded using a VAS of 0-3. RESULTS: In the first hour after discontinuing propofol and trial infusion, morphine requirements were significantly higher in the remifentanil group (8.15 (sd 3.59) mg) compared with the saline group (3.29 (2.36) mg) (P less than 0.01). There was no difference in the total morphine given during the period after stopping propofol or in the total requirement in the first 12 h postoperatively. There was no significant difference in either pain scores or agitation scores between the two groups. CONCLUSION: Use of remifentanil is associated with increased opioid requirement in the first hour after it has been discontinued." style="color:green">Rauf K et. al. Br J Anaesth 95: 611, 2005</balloon>]

-	A study of 30 adolescents with scoliosis randomized them to continuous remifentanil vs. intermittent morphine boluses during scoliosis surgery. All patients were placed on a morphine PCA post-operatively. At 24 hours, the remifentanil group had consumed 30% more opiates than the intraoperative morphine group, although there were no differences in pain or sedation scores, thus the increased morphine consumption, while statistically significant, may not be clinically significant [<balloon title="We tested the hypothesis that continuous intraoperative infusion of remifentanil is associated with the development of clinically relevant acute opioid tolerance in adolescents undergoing scoliosis surgery. Thirty adolescents were randomly assigned to receive an intraoperative analgesic regimen consisting of continuous remifentanil infusion or intermittent morphine alone. Postoperative analgesic consumption was assessed with a patient-controlled analgesia device that was used to self-administer morphine. Cumulative postoperative morphine consumption, pain scores, and sedation scores were recorded by a blinded investigator every hour for the first 4 h postoperatively and then every 4 h for a total of 24 h. Cumulative morphine consumption in the remifentanil group was significantly more than that in the morphine group at each time point in the initial 24 h after surgery (P less than 0.0001). At 24 h after surgery, cumulative morphine consumption was 30% greater in the remifentanil group (1.65 +/- 0.41 mg/kg) than in the morphine group (1.27 +/- 0.32 mg/kg) (95% confidence interval for the difference, 0.11 to 0.65 mg/kg). Differences in pain and sedation scores were not statistically significant. These data suggest that intraoperative infusion of remifentanil is associated with the development of clinically relevant acute opioid tolerance in adolescents undergoing scoliosis surgery" style="color:green">Crawford MW et. al. Anesth Analg 102: 1662, 2006</balloon>]	+	A study of 30 adolescents with scoliosis randomized them to continuous remifentanil vs. intermittent morphine boluses during scoliosis surgery. All patients were placed on a morphine PCA post-operatively. At 24 hours, the remifentanil group had consumed 30% more opiates than the intraoperative morphine group, although there were no differences in pain or sedation scores, thus the increased morphine consumption, while statistically significant, may not be clinically significant [<balloon title="We tested the hypothesis that continuous intraoperative infusion of remifentanil is associated with the development of clinically relevant acute opioid tolerance in adolescents undergoing scoliosis surgery. Thirty adolescents were randomly assigned to receive an intraoperative analgesic regimen consisting of continuous remifentanil infusion or intermittent morphine alone. Postoperative analgesic consumption was assessed with a patient-controlled analgesia device that was used to self-administer morphine. Cumulative postoperative morphine consumption, pain scores, and sedation scores were recorded by a blinded investigator every hour for the first 4 h postoperatively and then every 4 h for a total of 24 h. Cumulative morphine consumption in the remifentanil group was significantly more than that in the morphine group at each time point in the initial 24 h after surgery (P less than 0.0001). At 24 h after surgery, cumulative morphine consumption was 30% greater in the remifentanil group (1.65 +/- 0.41 mg/kg) than in the morphine group (1.27 +/- 0.32 mg/kg) (95% confidence interval for the difference, 0.11 to 0.65 mg/kg). Differences in pain and sedation scores were not statistically significant. These data suggest that intraoperative infusion of remifentanil is associated with the development of clinically relevant acute opioid tolerance in adolescents undergoing scoliosis surgery" style="color:green">Crawford MW et. al. Anesth Analg 102: 1662, 2006</balloon>; [http://www.anesthesia-analgesia.org/content/102/6/1662.full FREE Full-text at Anesthesia & Analgesia]]

-	'''Data out of Favor:''' A multicenter, prospective, randomized study of 245 patients undergoing urologic or general surgery with remifentanil-based anesthesia were randomized to morphine at 0.15 mg/kg versus 0.25 mg/kg 30 minutes before the end of surgery. The high-dose group required less post-operative morphine in the PACU (0.10 mg/kg, versus 0.1 mg/kg, p < 0.01), but also had three episodes of respiratory depression. This study does not adequately address the issue of hyperalgesia as the time period for which pain scores and opiate consumption were measured (ie in the PACU) is well within the expected period of efficacy for the morphine given 30 minutes prior to closing [<balloon title="We evaluated the effect of perioperative administration of two doses of morphine for postoperative analgesia after remifentanil-based anesthesia. The prospective, randomized study included 245 patients from 33 centers. All patients were scheduled for abdominal or urological surgery lasting more than 1 h. General anesthesia used remifentanil as the perioperative opioid (1 microg/kg as a bolus then, 0.5 microg/kg as a continuous infusion). A morphine bolus of 0. 15 mg/kg (0.15-mg group) or 0.25 mg/kg (0.25-mg group) was administered 30 min before the end of surgery. In the postanesthesia care unit, pain scores for patients were evaluated by using behavioral pain scores of 1-3, verbal pain scores of 0-3, and visual analog scale scores of 0-10). Postoperative analgesia was obtained by a morphine titration (3 mg every 5 min). Demographic and surgery characteristics were similar in both groups. The delay for first demand of morphine was similar in the 0.15-mg and the 0.25-mg groups (26 [9-60] and 30 [10-60] min, respectively). The frequency of morphine titration was similar in both groups (75% and 66%, respectively). The amount of morphine used in the postanesthesia care unit was smaller in the 0.25-mg group (0.16 [0.0-1.25] vs 0.10 [0.0-0.56] mg/kg; P = 0.008). In the 0.25-mg group, the behavioral pain score was lower at 15 min, the verbal pain score was lower at 60 min (P less than 0.001), and similar at 30 min. The visual analog scale pain score at 30 min and 60 min was similar in both groups. The incidence of minor side effects was similar in both groups. However, three cases of postoperative respiratory depression occurred in the 0.25-mg group compared with no cases in the 0.15-mg group. In conclusion, perioperative administration of morphine alone does not provide entirely adequate immediate postoperative pain control after remifentanil-based anesthesia in major surgery. Implications: The administration of 0.15 or 0.25 mg/kg perioperative morphine during remifentanil-based anesthesia for major surgery does not preclude additional morphine administration in the postanesthesia care unit. The larger dose of 0.25 mg/kg slightly improves postoperative analgesia; however, it may be responsible for postoperative respiratory depression." style="color:green">Fletcher D et. al. Anesth Analg 90: 666, 2000</balloon>]	+	'''Data out of Favor:''' A multicenter, prospective, randomized study of 245 patients undergoing urologic or general surgery with remifentanil-based anesthesia were randomized to morphine at 0.15 mg/kg versus 0.25 mg/kg 30 minutes before the end of surgery. The high-dose group required less post-operative morphine in the PACU (0.10 mg/kg, versus 0.1 mg/kg, p < 0.01), but also had three episodes of respiratory depression. This study does not adequately address the issue of hyperalgesia as the time period for which pain scores and opiate consumption were measured (ie in the PACU) is well within the expected period of efficacy for the morphine given 30 minutes prior to closing [<balloon title="We evaluated the effect of perioperative administration of two doses of morphine for postoperative analgesia after remifentanil-based anesthesia. The prospective, randomized study included 245 patients from 33 centers. All patients were scheduled for abdominal or urological surgery lasting more than 1 h. General anesthesia used remifentanil as the perioperative opioid (1 microg/kg as a bolus then, 0.5 microg/kg as a continuous infusion). A morphine bolus of 0. 15 mg/kg (0.15-mg group) or 0.25 mg/kg (0.25-mg group) was administered 30 min before the end of surgery. In the postanesthesia care unit, pain scores for patients were evaluated by using behavioral pain scores of 1-3, verbal pain scores of 0-3, and visual analog scale scores of 0-10). Postoperative analgesia was obtained by a morphine titration (3 mg every 5 min). Demographic and surgery characteristics were similar in both groups. The delay for first demand of morphine was similar in the 0.15-mg and the 0.25-mg groups (26 [9-60] and 30 [10-60] min, respectively). The frequency of morphine titration was similar in both groups (75% and 66%, respectively). The amount of morphine used in the postanesthesia care unit was smaller in the 0.25-mg group (0.16 [0.0-1.25] vs 0.10 [0.0-0.56] mg/kg; P = 0.008). In the 0.25-mg group, the behavioral pain score was lower at 15 min, the verbal pain score was lower at 60 min (P less than 0.001), and similar at 30 min. The visual analog scale pain score at 30 min and 60 min was similar in both groups. The incidence of minor side effects was similar in both groups. However, three cases of postoperative respiratory depression occurred in the 0.25-mg group compared with no cases in the 0.15-mg group. In conclusion, perioperative administration of morphine alone does not provide entirely adequate immediate postoperative pain control after remifentanil-based anesthesia in major surgery. Implications: The administration of 0.15 or 0.25 mg/kg perioperative morphine during remifentanil-based anesthesia for major surgery does not preclude additional morphine administration in the postanesthesia care unit. The larger dose of 0.25 mg/kg slightly improves postoperative analgesia; however, it may be responsible for postoperative respiratory depression." style="color:green">Fletcher D et. al. Anesth Analg 90: 666, 2000</balloon>; [http://www.anesthesia-analgesia.org/content/90/3/666.full FREE Full-text at Anesthesia & Analgesia]]

	A study of 60 elective open gynecological surgery patients randomized them to remifentanil (mean 0.24 ucg/kg/min) vs. sevoflurane-based (mean 1.75% inspired) anesthesia. All patients received a PCA post-operatively. The remifentanil group used 28.0 mg (versus 28.6 mg in the sevoflurane group, NS) at 24 hours. Pain scores were similar [<balloon title="We have prospectively assessed whether remifentanil-based anaesthesia is associated with clinically relevant acute opioid tolerance, expressed as greater postoperative pain scores or morphine consumption. Sixty patients undergoing elective gynaecological, non-laparoscopic, surgery were randomly assigned to receive remifentanil (group R, n=30) or sevoflurane (group S, n=30) based anaesthesia. Postoperative analgesia was provided with morphine through a patient-controlled infusion device. Mean (SD) remifentanil infusion rate in group R was 0.23 (0.10) microg kg(-1) min(-1) and mean inspired fraction of sevoflurane in group S was 1.75 (0.70)%. Mean (SD) cumulative morphine consumption during the first 24 postoperative hours was similar between groups: 28.0 (14.2) mg (group R) vs 28.6 (12.4) mg (group S). Pain scores, were also similar between groups during this period. These data do not support the development of acute opioid tolerance after remifentanil-based anaesthesia in this type of surgery" style="color:green">Cortínez LI et. al Br J Anaesth 87: 866, 2001</balloon>]		A study of 60 elective open gynecological surgery patients randomized them to remifentanil (mean 0.24 ucg/kg/min) vs. sevoflurane-based (mean 1.75% inspired) anesthesia. All patients received a PCA post-operatively. The remifentanil group used 28.0 mg (versus 28.6 mg in the sevoflurane group, NS) at 24 hours. Pain scores were similar [<balloon title="We have prospectively assessed whether remifentanil-based anaesthesia is associated with clinically relevant acute opioid tolerance, expressed as greater postoperative pain scores or morphine consumption. Sixty patients undergoing elective gynaecological, non-laparoscopic, surgery were randomly assigned to receive remifentanil (group R, n=30) or sevoflurane (group S, n=30) based anaesthesia. Postoperative analgesia was provided with morphine through a patient-controlled infusion device. Mean (SD) remifentanil infusion rate in group R was 0.23 (0.10) microg kg(-1) min(-1) and mean inspired fraction of sevoflurane in group S was 1.75 (0.70)%. Mean (SD) cumulative morphine consumption during the first 24 postoperative hours was similar between groups: 28.0 (14.2) mg (group R) vs 28.6 (12.4) mg (group S). Pain scores, were also similar between groups during this period. These data do not support the development of acute opioid tolerance after remifentanil-based anaesthesia in this type of surgery" style="color:green">Cortínez LI et. al Br J Anaesth 87: 866, 2001</balloon>]

Droperidol (Controversies)

2010-09-02T14:43:46Z

←Older revision		Revision as of 14:43, 2 September 2010
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	''Review of Documented Cases: Habib et. al.''		''Review of Documented Cases: Habib et. al.''

-	The FDA warning is based on 10 reported cases from 1997-2002 [<balloon title="Abstract not available [letter], please see Pubmed for link to complete article (free text online)" style="color:green">Habib et. al. ~~Anesthesia and Analgesia~~ 96: 1377, 2003</balloon>] - these 10 cases were all with 1.25 mg or less.	+	The FDA warning is based on 10 reported cases from 1997-2002 [<balloon title="Abstract not available [letter], please see Pubmed for link to complete article (free text online)" style="color:green">Habib et. al. Anesth Analg 96: 1377, 2003</balloon>; [http://www.anesthesia-analgesia.org/content/96/5/1377.full FREE Full-text at Anesthesia & Analgesia]] - these 10 cases were all with 1.25 mg or less.

	'''Data in Favor of Droperidol Use:'''		'''Data in Favor of Droperidol Use:'''
Line 13:		Line 13:
	''Review of Documented Cases: Habib et. al.''		''Review of Documented Cases: Habib et. al.''

-	In none of the 10 cases with 1.25 mg or less could a definitive cause-effect relationship be described, and in five of them there were substantial confounding factors. Assuming that droperidol sales averaged 11 MM ampules per year, and that these events were truly related to droperidol, the authors estimated that the incidence of associated events was 1:150,000 [Habib et. al. ~~Anesthesia and Analgesia~~ 96: 1377, 2003]	+	In none of the 10 cases with 1.25 mg or less could a definitive cause-effect relationship be described, and in five of them there were substantial confounding factors. Assuming that droperidol sales averaged 11 MM ampules per year, and that these events were truly related to droperidol, the authors estimated that the incidence of associated events was 1:150,000 [<balloon title="Abstract not available [letter], please see Pubmed for link to complete article (free text online)" style="color:green">Habib et. al. Anesth Analg 96: 1377, 2003</balloon>; [http://www.anesthesia-analgesia.org/content/96/5/1377.full FREE Full-text at Anesthesia & Analgesia]]

	''Charbit et. al.''		''Charbit et. al.''

-	A small study compared QT prolongation with droperidol alone, ondansetron alone, and both combined. Both droperidol and ondansetron significantly prolonged QT interval as expected (droperidol>ondansetron), but when combined did not prolong QT significantly more than droperidol alone {Charbit et. al. Anesthesiology 109: 206, 2008}	+	A small study compared QT prolongation with droperidol alone, ondansetron alone, and both combined. Both droperidol and ondansetron significantly prolonged QT interval as expected (droperidol>ondansetron), but when combined did not prolong QT significantly more than droperidol alone [Charbit et. al. Anesthesiology 109: 206, 2008]

	''Chu et. al.''		''Chu et. al.''

-	400 total patients (randomized, prospective, controlled) studied haloperidol plus dexamethasone on PONV versus placebo and droperidol alone in vaginal hysterectomy patients. Haloperidol plus dexamethasone produced the greatest reduction in PONV when compared to placebo, either drug alone, or droperidol alone. There was no difference in QT prolongation in the haloperidol plus dexamethasone vs. droperidol alone {Chu et. al. Anesth Analg 106: 1402, 2008}	+	400 total patients (randomized, prospective, controlled) studied haloperidol plus dexamethasone on PONV versus placebo and droperidol alone in vaginal hysterectomy patients. Haloperidol plus dexamethasone produced the greatest reduction in PONV when compared to placebo, either drug alone, or droperidol alone. There was no difference in QT prolongation in the haloperidol plus dexamethasone vs. droperidol alone [<balloon title="BACKGROUND: Haloperidol, a major tranquilizer, has been found to have a potent antiemetic effect on postoperative nausea and vomiting (PONV), but the prophylactic effect of haloperidol plus dexamethasone on PONV has not been evaluated. We evaluated the prophylactic effect of haloperidol plus dexamethasone to either given alone, placebo or droperidol on PONV in patients undergoing a laparoscopic-assisted vaginal hysterectomy.
		+
		+	METHODS: Four hundred adult women (n = 80 in each of five groups) scheduled for a laparoscopic-assisted vaginal hysterectomy were enrolled in a randomized, double-blind, placebo, and positive-control study. Fifteen minutes after the induction of anesthesia, patients received an IV injection of either saline (group S), droperidol 1.25 mg (group D), haloperidol 2 mg (group H), dexamethasone 5 mg (group Dx), or haloperidol 2 mg plus dexamethasone 5 mg (group H + Dx) to prevent PONV. The occurrence of PONV and medication-related side effects were recorded.
		+
		+	RESULTS: The incidences of PONV (0–24 h) in the D (36%), H (37%), Dx (38%), and H + Dx (19%) groups were significantly lower than in the S group (65%; P less than 0.05 for each comparison). The H + Dx group had the lowest incidence of PONV (19%; P less than 0.05 for each comparison) of the five study groups. No differences were found between the D, H, and Dx groups. Also, no differences were found among the five groups in the side effects of QT prolongation, intensity of postoperative pain, level of sedation, and occurrence of extra-pyramidal symptoms.
		+
		+	CONCLUSION: Prophylactic haloperidol 2 mg plus dexamethasone 5 mg produced a greater reduction in the incidence of PONV than did either drug used alone, placebo or droperidol without increasing perioperative adverse outcomes. " style="color:green">Chu CC et al. Anesth Analg 106: 1402, 2008</balloon>]; [http://www.anesthesia-analgesia.org/content/106/5/1402.full FREE Full-text at Anesthesia & Analgesia].

	''Nuttal et. al.''		''Nuttal et. al.''

-	Lastly, a retrospective study in Anesthesiology studied whether or not droperidol (low dose) administration increased the incidence of torsades during a 3 year period before and after the FDA placed the black box warning on the drug. They determined that there was no change in the incidence of torsades with the use of low dose droperidol versus none used. The incidence of torsades in droperidol exposure was found to be 1:16791, and the one incident may not have actually been due to droperidol {Nuttal et. al. Anesthesiology 107: 531, 2007}	+	Lastly, a retrospective study in Anesthesiology studied whether or not droperidol (low dose) administration increased the incidence of torsades during a 3 year period before and after the FDA placed the black box warning on the drug. They determined that there was no change in the incidence of torsades with the use of low dose droperidol versus none used. The incidence of torsades in droperidol exposure was found to be 1:16791, and the one incident may not have actually been due to droperidol [Nuttal et. al. Anesthesiology 107: 531, 2007]

	'''Summary:'''		'''Summary:'''

Template:Methylene blue

2010-09-02T14:32:56Z

Cardiopulmonary Bypass:

←Older revision		Revision as of 14:32, 2 September 2010
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	Ozal et al. randomized patients “at risk” for post-operative vasoplegia (undergoing CABG procedures and having taken ACE-inhibitors, calcium channel blockers, or heparin preoperatively) to 2 mg/kg '''methylene blue''' versus nothing (no placebo). The two groups differed in the incidence of vasoplegia (0% vs. 26%, p < 0.001), average ICU stay (1.2 vs. 2.1 days, p < 0.001), and average hospitalization (6.1 vs. 8.4 days, p < 0.001). The methylene blue group required less volume (1.57 L vs. 1.75 L, p = 0.024), displayed higher SVR (p < 0.001), had lower ionotropic requirements to come off of bypass (p < 0.001), and had higher urine output during bypass (738 vs 631 cc, p = 0.019) despite a trend towards lower time on bypass (68.5 vs 70.7 minutes, p = 0.123) [<balloon title="BACKGROUND: Angiotensin-converting enzyme inhibitors, calcium channel blockers, and preoperative intravenous heparin use are independent risk factors for vasoplegic syndrome after cardiac surgery. We prospectively studied whether preoperative methylene blue administration would prevent the vasoplegic syndrome in these high-risk patients. METHODS: One hundred patients scheduled for coronary artery bypass graft surgery who were at high risk for vasoplegia because they were preoperatively using angiotensin-converting enzyme inhibitors, calcium channel blockers, and heparin were randomly assigned to either receive preoperative methylene blue (group 1, n = 50) or not receive it (group 2, controls, n = 50). Methylene blue (1% solution) was administered intravenously at a dose of 2 mg/kg for more than 30 minutes, beginning in the intensive care unit 1 hour before surgery. RESULTS: Although similar in terms of all demographic and operative variables, the two groups differed significantly in terms of vasoplegic syndrome incidence (0% in group 1[0 of 50] vs 26% in group 2 [13 of 50]; p less than 0.001). In 6 patients, the vasoplegic syndrome was refractory to norepinephrine. Four of these patients survived; the other 2 had vasoplegic syndromes that were refractory to aggressive vasopressor therapy, and they ultimately died of multiorgan failure. Stroke occurred in 1 patient. The two study groups also differed significantly in terms of average intensive care unit stay (1.2 +/- 0.5 days in group 1 vs 2.1 +/- 1.2 days in group 2; p less than 0.001) and average hospital stay (6.1 +/- 1.7 days in group 1 vs 8.4 +/- 2.0 days in group 2; p less than 0.001). CONCLUSIONS: Our results suggest that preoperative methylene blue administration reduces the incidence and severity of vasoplegic syndrome in high-risk patients, thus ensuring adequate systemic vascular resistance in both operative and postoperative periods and shortening both intensive care unit and hospital stays" style="color:green">Ozal E et al. Ann Thorac Surg 79: 1615, 2005</balloon>]		Ozal et al. randomized patients “at risk” for post-operative vasoplegia (undergoing CABG procedures and having taken ACE-inhibitors, calcium channel blockers, or heparin preoperatively) to 2 mg/kg '''methylene blue''' versus nothing (no placebo). The two groups differed in the incidence of vasoplegia (0% vs. 26%, p < 0.001), average ICU stay (1.2 vs. 2.1 days, p < 0.001), and average hospitalization (6.1 vs. 8.4 days, p < 0.001). The methylene blue group required less volume (1.57 L vs. 1.75 L, p = 0.024), displayed higher SVR (p < 0.001), had lower ionotropic requirements to come off of bypass (p < 0.001), and had higher urine output during bypass (738 vs 631 cc, p = 0.019) despite a trend towards lower time on bypass (68.5 vs 70.7 minutes, p = 0.123) [<balloon title="BACKGROUND: Angiotensin-converting enzyme inhibitors, calcium channel blockers, and preoperative intravenous heparin use are independent risk factors for vasoplegic syndrome after cardiac surgery. We prospectively studied whether preoperative methylene blue administration would prevent the vasoplegic syndrome in these high-risk patients. METHODS: One hundred patients scheduled for coronary artery bypass graft surgery who were at high risk for vasoplegia because they were preoperatively using angiotensin-converting enzyme inhibitors, calcium channel blockers, and heparin were randomly assigned to either receive preoperative methylene blue (group 1, n = 50) or not receive it (group 2, controls, n = 50). Methylene blue (1% solution) was administered intravenously at a dose of 2 mg/kg for more than 30 minutes, beginning in the intensive care unit 1 hour before surgery. RESULTS: Although similar in terms of all demographic and operative variables, the two groups differed significantly in terms of vasoplegic syndrome incidence (0% in group 1[0 of 50] vs 26% in group 2 [13 of 50]; p less than 0.001). In 6 patients, the vasoplegic syndrome was refractory to norepinephrine. Four of these patients survived; the other 2 had vasoplegic syndromes that were refractory to aggressive vasopressor therapy, and they ultimately died of multiorgan failure. Stroke occurred in 1 patient. The two study groups also differed significantly in terms of average intensive care unit stay (1.2 +/- 0.5 days in group 1 vs 2.1 +/- 1.2 days in group 2; p less than 0.001) and average hospital stay (6.1 +/- 1.7 days in group 1 vs 8.4 +/- 2.0 days in group 2; p less than 0.001). CONCLUSIONS: Our results suggest that preoperative methylene blue administration reduces the incidence and severity of vasoplegic syndrome in high-risk patients, thus ensuring adequate systemic vascular resistance in both operative and postoperative periods and shortening both intensive care unit and hospital stays" style="color:green">Ozal E et al. Ann Thorac Surg 79: 1615, 2005</balloon>]

-	Maslow et al. randomized 31 patients who had received ACE-inhibitors and who were undergoing cardiopulmonary bypass (CPB) to 3 mg/kg of '''methylene blue''' versus saline following CPB and cardioplegia. Methylene blue increased MAPs (statistically significant at post-drug and 20-40 mins of CPB timepoints, but not at 60 minutes of CPB or post-CPB) and SVR (significant up to 40 minutes), thus the effects appeared to last only ~ 40 minutes. Methylene blue administration resulted in lower phenylephrine and norephrine requirements, and resulted in lower serum lactate levels. While the methylene blue group had higher cardiac output post-bypass (6.1 L/m vs. 5.6 L/min), this did not reach statistical significance [<balloon title="Hypotension occurs during cardiopulmonary bypass (CPB), in part because of induction of the inflammatory response, for which nitric oxide and guanylate cyclase play a central role. In this study we examined the hemodynamic effects of methylene blue (MB), an inhibitor of guanylate cyclase, administered during cardiopulmonary bypass (CPB) to patients taking angiotensin-converting enzyme inhibitors. Thirty patients undergoing cardiac surgery were randomized to receive either MB (3 mg/kg) or saline (S) after institution of CPB and cardioplegic arrest. CPB was managed similarly for all study patients. Hemodynamic data were assessed before, during, and after CPB. The use of vasopressors was recorded. All study patients experienced a similar reduction in mean arterial blood pressure (MAP) and systemic vascular resistance (SVR) with the onset of CPB and cardioplegic arrest. MB increased MAP and SVR and this effect lasted for 40 minutes. The saline group demonstrated a persistently reduced MAP and SVR throughout CPB. The saline group received phenylephrine more frequently during CPB, and more norepinephrine after CPB to maintain a desirable MAP. The MB group recorded significantly lower serum lactate levels despite equal or greater MAP and SVR. In conclusion, administration of MB after institution of CPB for patients taking angiotensin-converting enzyme inhibitors increased MAP and SVR and reduced the need for vasopressors. Furthermore, serum lactate levels were lower in MB patients, suggesting more favorable tissue perfusion" style="color:green">Maslow AD et al. Anesth Analg 103: 2, 2006</balloon>]	+	Maslow et al. randomized 31 patients who had received ACE-inhibitors and who were undergoing cardiopulmonary bypass (CPB) to 3 mg/kg of '''methylene blue''' versus saline following CPB and cardioplegia. Methylene blue increased MAPs (statistically significant at post-drug and 20-40 mins of CPB timepoints, but not at 60 minutes of CPB or post-CPB) and SVR (significant up to 40 minutes), thus the effects appeared to last only ~ 40 minutes. Methylene blue administration resulted in lower phenylephrine and norephrine requirements, and resulted in lower serum lactate levels. While the methylene blue group had higher cardiac output post-bypass (6.1 L/m vs. 5.6 L/min), this did not reach statistical significance [<balloon title="Hypotension occurs during cardiopulmonary bypass (CPB), in part because of induction of the inflammatory response, for which nitric oxide and guanylate cyclase play a central role. In this study we examined the hemodynamic effects of methylene blue (MB), an inhibitor of guanylate cyclase, administered during cardiopulmonary bypass (CPB) to patients taking angiotensin-converting enzyme inhibitors. Thirty patients undergoing cardiac surgery were randomized to receive either MB (3 mg/kg) or saline (S) after institution of CPB and cardioplegic arrest. CPB was managed similarly for all study patients. Hemodynamic data were assessed before, during, and after CPB. The use of vasopressors was recorded. All study patients experienced a similar reduction in mean arterial blood pressure (MAP) and systemic vascular resistance (SVR) with the onset of CPB and cardioplegic arrest. MB increased MAP and SVR and this effect lasted for 40 minutes. The saline group demonstrated a persistently reduced MAP and SVR throughout CPB. The saline group received phenylephrine more frequently during CPB, and more norepinephrine after CPB to maintain a desirable MAP. The MB group recorded significantly lower serum lactate levels despite equal or greater MAP and SVR. In conclusion, administration of MB after institution of CPB for patients taking angiotensin-converting enzyme inhibitors increased MAP and SVR and reduced the need for vasopressors. Furthermore, serum lactate levels were lower in MB patients, suggesting more favorable tissue perfusion" style="color:green">Maslow AD et al. Anesth Analg 103: 2, 2006</balloon>; [http://www.anesthesia-analgesia.org/content/103/1/2.full FREE Full-text at Anesthesia & Analgesia]]