Your brain under anesthesia

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Anesthesiology 10 2015, Vol.123, 937-960. Clinical Electroencephalography for Anesthesiologists: Part I: Background and Basic Signatures
Patrick L. Purdon, Ph.D.; Aaron Sampson, B.S.; Kara J. Pavone, B.S.; Emery N. Brown, M.D., Ph.D.

Unprocessed electroencephalogram signatures of propofol-induced sedation and unconsciousness. (A) Awake eyes open electroencephalogram pattern. (B) Paradoxical excitation. (C) Alpha and beta oscillations commonly observed during propofol-induced sedation (fig. 5). (D) Slow-delta and alpha oscillations commonly seen during unconsciousness. (E) Slow oscillations commonly observed during unconsciousness at induction with propofol (fig. 6) and sedation with dexmedetomidine (fig. 11) and with nitrous oxide (fig. 13). (F) Burst suppression, a state of profound anesthetic-induced brain inactivation commonly occurring in elderly patients,68 anesthetic-induced coma, and profound hypothermia (fig. 6, B and D). (G) Isoelectric electroencephalogram pattern commonly observed in anesthetic-induced coma and profound hypothermia. With the exception of the isoelectric state, the amplitudes of the electroencephalogram signatures of the anesthetized states are larger than the amplitudes of the electroencephalogram in the awake state by a factor of 5 to 20. All electroencephalogram recordings are from the same subject. Reproduced, with permission, from Brown et al. Chapter 50 in Miller’s Anesthesia, 8th edition, 2014.


The brain on propofol.  

A is adapted, with permission, from Purdon et al:Electroencephalogram signatures of loss and recovery of consciousness from propofol. Proc Natl Acad Sci U S A 2013; 110:E1142–51; and C is adapted, with permission, from Lewis et al. Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness. Proc Natl Acad Sci U S A2012; 109:E3377–86. Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


(A) At low doses, ketamine blocks preferentially the actions of glutamate N-methyl-d-aspartate receptors on γ-aminobutyric acid (GABA)ergic inhibitory interneurons in the cortex and subcortical sites such as the thalamus, hippocampus, and the limbic system. The antinociceptive effect of ketamine is due in part to its blockade of glutamate release from peripheral afferent (PAF) neurons in the dorsal root ganglia (DRG) at their synapses on to projection neurons (PNs) in the spinal cord. (B) Spectrogram showing the beta-gamma oscillations in the electroencephalogram of a 61-yr-old woman who received ketamine administered in 30 mg and 20 mg doses (green arrows) for a vacuum dressing change. Blocking the inhibitory action of the interneurons in cortical and subcortical circuits helps explain why ketamine produces beta oscillations as its electroencephalogram signature. (C) Ten-second electroencephalogram trace recorded at minute 5 from the spectrogram in B. A is reproduced, with permission, from Brown, Purdon, and Van Dort: General anesthesia and altered states of arousal: A systems neuroscience analysis. Annu Rev Neurosci. 2011;324:601–28. B and C were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission, from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Spectrograms and time domain electroencephalogram signatures of dexmedetomidine-induced sedation. (A) Spectrogram of the electroencephalogram of a 59-kg patient receiving a 0.65 μg kg−1 h−1 dexmedetomidine infusion to maintain sedation. The spectrogram shows spindles (9 to 15 Hz oscillations) and slow-delta oscillations. (B) Ten-second electroencephalogram trace recorded at minute 60 from the spectrogram in A emphasizing spindles (red underlines). (C) Spectrogram of the electroencephalogram of a 65-kg patient receiving a 0.85 μg kg−1 h−1 dexmedetomidine infusion to maintain sedation. (D) Ten-second electroencephalogram trace recorded at minute 40 from the spectrogram in C showing the slow-delta oscillations. A–D were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Spectrograms and time domain electroencephalogram signatures of sevoflurane, isoflurane, and desflurane at surgical levels of unconsciousness. The inspired concentration of the anesthetics is the blue trace in the upper part of each panel. Green arrows below each panel are propofol bolus doses. (A) At sub-minimal alveolar concentrations (MACs) (minutes 40 to 60), the spectrogram of sevoflurane resembles that of propofol (fig. 6, A and B). As the concentration of sevoflurane is increased (minutes 100 to 120), theta (5 to 7Hz) oscillations appear. The theta oscillations dissipate when the sevoflurane concentration (blue curve) is decreased. (B) Ten-second electroencephalogram trace of sevoflurane recorded at minute 40 of the spectrogram in A. (C) The spectrogram of sevoflurane shows constant alpha, slow, delta and theta oscillations at a constant concentration of 3%. (D) Ten-second electroencephalogram trace of sevoflurane recorded at minute 30 of the spectrogram in C. (E) At sub-MAC concentrations (minutes 16 to 26), the spectrogram of isoflurane resembles that of propofol (fig. 6, A and B) and sub-MAC sevoflurane (A). Theta oscillations strengthen as the isoflurane concentration increases toward MAC. (F) Ten-second electroencephalogram trace of isoflurane recorded at minute 40 of the spectrogram in E. (G) At the sub-MAC concentrations shown here, the spectrogram of desflurane resembles propofol with very low theta oscillation power. (H) Ten-second electroencephalogram trace of isoflurane recorded at minute 40 of the spectrogram in G. A, C, E, and G were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Slow-delta and beta-gamma oscillations associated with nitrous oxide. (A) Prior to emergence, a patient was maintained on 0.5% isoflurane and 58% oxygen. At minute 82, the composition of the anesthetic gases was changed to 0.2% isoflurane (blue curve) in 75% nitrous oxide (green curve) and 24% oxygen. The total gas flow was increased from 3 to 7 l/min. The alpha, theta, and slow oscillation power decreased from minutes 83 to 85. At minute 86, the power in the theta to beta bands decreased considerably (blue area) as the slow-delta oscillation power increased. At minute 89, the slow-delta oscillation power decreased and the beta-gamma oscillations appeared at minute 90. The flow rates and anesthetic concentrations were maintained constant between minutes 82 and 91. Isoflurane was turned off at minute 91. (B) Ten-second electroencephalogram traces of the slow-delta oscillation at minute 86.7 and the beta-gamma oscillations at minute 90.8. A and B were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Different anesthetics (propofol, sevoflurane, ketamine, and dexmedetomidine), different electroencephalogram signatures, and different molecular and neural circuit mechanisms. (A) Anesthetic-specific differences in the electroencephalogram are difficult to discern in unprocessed electroencephalogram waveforms. (B) In the spectrogram, it is clear that different anesthetics produce different electroencephalogram signatures. The dynamics the electroencephalogram signatures can be related to the molecular targets and the neural circuits at which the anesthetics act to create altered states of arousal. Propofol and sevoflurane enhance γ-aminobutyric acid (GABA)ergic inhibition, sevoflurane binds at GABA receptors and other molecular targets, ketamine blocks N-methyl-d-aspartate (NMDA) glutamate receptors, and dexmedetomidine is a presynaptic alpha adrenergic agonist. A and B were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Key points:

  • For the inhaled ether-derived anesthetics such as sevoflurane, isoflurane, and desflurane, we observed that, with the exception of the theta oscillations that appear around 1 MAC and beyond, their electroencephalogram patterns during maintenance and emergence closely resemble those seen in propofol. Nitrous oxide is known to be associated with increased beta and gamma oscillations and likely decreased slow-delta oscillations. However, we demonstrated that nitrous oxide also produces profound slow-delta oscillations during the transition from an inhaled ether anesthetic.
  • An animated version of portions of parts I and II are available at www.AnesthesiaEEG.com.

How Should We Manage PAR After TAVI?

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invasivecardiology

Stefan Toggweiler, MD

Evidence indicates that postprocedural moderate or severe paravalvular regurgitation (PAR) reduces life expectancy in such a way that it may even nullify the beneficial effect of TAVI.
Due to improved implantation techniques, knowledge, and materials, the rates of moderate or severe PAR have dropped to less than 5%-10% in most recently published trials and registries, but mild PAR still occurs quite frequently. Many interventional cardiologists now aim for the “perfect” result, and even mild PAR seems to justify postdilatation of a transcatheter valve. However, we should keep in mind that postdilatation carries the risks of annular injury, valve displacement, and embolization of calcific debris.
In our study published in the month’s JIC, we investigated the natural course of PAR after implantation of the self-expandable CoreValve. Patients underwent transesophageal echocardiography after 30 days and 1 year. In most patients, PAR improved. Very small jets disappeared, and larger…

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Awake Tracheostomy

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They say that anesthesiology is 95% comfy and relaxed and the other 5% is “oh shit”!  It’s a great career choice — pretty flexible hours, great patient contact, broad spectrum medicine, crisis management, leadership role, etc.

There happened to be an interesting case in the OR — awake tracheostomy for a patient coming in from home.

What’s a tracheotomy?

Evaluation of the airway PPT

The Difficult Airway in Head and Neck Tumor Surgery

Anesthesia for tracheostomy for huge maxillofacial tumor. From SJA: CASE REPORT Year : 2014 | Volume : 8 | Issue : 1 | Page : 124-127

Our patient had two prior tracheotomies all with successful decannulation.  His most recent trach was about 2.5 months ago (which a fiberoptic intubation was used with a 6.0 ETT).   He had a neck cancer with a rapidly growing tongue base tumor that seems to be less responsive to chemo than his shrinking neck tumor.  Because of the enlarging size of the tongue base tumor, he is starting to notice worsening stridor without his trach.  The ENT surgeon evaluated his airway just days before and deemed it unintubateable.  Therefore, my plan was to have a pedi FO scope with 5.0 cuffed ETT (smallest available in our OR), glidescope, emergency cric supplies (14g angio cath, 3cc syringe with plunger removed and 7.0 ETT adapter hooked into the end of the syringe), jet ventilator and tubes, and ENT surgeon.

We decided to use a bit of midazolam as well as Precedex for the awake trach.  The dosing on the package says 1 mcg/kg for 10 minutes then 0.7 mcg/kg/hr.  We started with 0.5 mcg/kg for 10 minutes then 0.5 mcg/kg/hr.  This regimen worked well as we started it in preop and monitored his SpO2 as he dozed off but was easily aroused to voice and gentle touch.

The Role of Dexmedetomidine for Awake Trach

Monitors were placed in the OR and we used a face mask running 10 L/min O2 with ETCO2 monitoring.  Every now and then he would obstruct while lying supine, therefore, we placed a nasal trumpet to aid the obstruction.  The surgeon localized the surgical area. See video for procedure.

The patient coughed once the trachea was perforated, but it was short lived as the surgeons were able to place the trach and hookup to our anesthesia circuit.  After confirming ETCO2, we pushed propofol IV and the remainder of the case was performed under general anesthesia (direct laryngoscopy and biopsy by surgeon).

Key take home points

  • Effective communication with the patient pre-op: expectations, sedation, potential complications.
  • Arm yourself! Do this like you would a difficult airway! Fiberoptic intubation supplies, glidescope, emergency cricothyroidotomy supplies, backup LMA, extra hands on deck (grab your anesthesia colleagues, anesthesia techs, extra help!), ENT… it never hurts to be over prepared!
  • Deliberate, effective communication with the ENT colleague across the drape.
  • Document any intubation performed, tools used, trachs placed so your anesthesia colleagues will know what worked in the past to secure an airway.
  • Breathe a sigh of relief bc these kind of cases are extremely uncommon!  Pat yourself on the back for a job well-done!

Now check out this amazing Case Report on a patient with a massive maxillofacial tumor!