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.
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.
- 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.
Originally posted on 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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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.
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.
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!
This article is quite a bit antiquated, but touches on some good basic points in cardiac anesthesia for CABG.