BISPECTRAL INDEX

💆The EEG bispectrum is a high-order statistical computation derived from the analog EEG.

💆The BIS is a combination of three weighted parameters: (i) the burst suppression ratio (the proportion of isoelectric EEG signal in an epoch); (ii) the beta ratio (a measure of the proportion of signal power in the high vs medium frequency range); and (iii) the SynchFastSlow (relative synchrony of fast and slow waves)

💆Changes in frequency and power alone ( as done with conventional power spectral analysis) have been shown to be inconsistent when attempting to measure anesthetic depth.

💆Bispectral analysis incorporates information on power and frequency with the phase coupling information that is more indicative of anesthetic depth but not present in other clinical applications of EEG.

💆The BIS uses a combination of EEG subparameters that were selected after analysis of a large database of EEGs to demonstrate specific ranges for varying phases of anesthetic effect

💆These parameters were then combined to form the optimum configuration for monitoring of the hypnotic state.

💆The BIS is then displayed as a dimensionless number between 0 and 100 with the lower numbers corresponding to deeper levels of hypnosis.

💆There are normal, genetically determined low-voltage EEG variants among the population that can result in abnormally low BIS values in awake patients; therefore, it is important to obtain baseline values before the induction of anesthesia

💆BIS is not able to predict movement in response to surgical stimulation because the generation of reflexes is likely to be at spinal cord rather than cortical level

💆BIS does not fully reflect the synergistic effect of opioids with hypnotic agents

💆The presence of electromyographic artefacts, poor signal quality, and electrical artefacts such as those from electro-cautery and forced air warming units can cause spurious values to be displayed by the BIS monitor.

💆With the administration of ketamine, the BIS may remain high, possibly due to the excitatory actions of ketamine, and, therefore, the BIS monitor is not reliable when used to monitor hypnosis with ketamine.

💆There have been studies in which the BIS monitor has not been shown to reflect the hypnotic contribution to the anesthetic by nitrous oxide.

💆Potential benefits from the routine use of the BIS monitor include

➖decreased risk of awareness

➖improved titration of anesthetic agents and

➖decreased recovery room time

💆The BIS also gives the anesthetist additional information to consider when selecting drugs for interventions, for example, when making the decision whether to deepen anesthesia with a volatile agent, add more analgesia with an opioid, or use a vasoactive drug.

💆Also note:

➖The BIS may drop after giving a neuromuscular blocking agent if excessive EMG was present prior to giving it.

➖Ischemia attenuates the amplitude and frequency of the EEG signal, which may result in a decrease in BIS

➖Hypothermia decreases brain activity, and may decrease BIS

➖Muscle shivering, tightening, twitching etc may increase EMG and increase BIS

➖Artifacts in the higher frequency ranges [e.g. use of any mechanical device that could generate high frequency activity like patient warmer]can artificially increase the BIS value

➖Is the BIS decreasing when you think it should be increasing? Think of Paradoxical Delta pattern (characterized by a pronounced slowing of the EEG) which occurs over a short period of time (2-3 minutes).

➖If the sensor is placed over the temporal artery, pulse artifacts can cause the BIS value to be inappropriately low. Check EEG waveform for presence of pulse artifacts and move sensor if necessary.

➖Blinking or rolling his/her head by the patient, may cause artifacts that mimic slow frequency EEG patterns.

Reference: The BIS monitor: A review and technology assessment, James W. Bard, AANA Journal/December 2001/Vol. 69, No. 6

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

😐(Explicit = Fully and clearly expressed)

😐(Implicit =Implied or understood though not directly expressed)

😐The incidence of awareness is around 0.1–0.2%

😐Explicit Awareness is intentional or conscious recollection of prior experiences as assessed by tests or recall or recognition, which are also called direct memory test.

😐Implicit Awareness is perception without conscious recall. The patient denies recall, but may remember “something” under hypnosis.

😐Awareness (deliberate)
Surgery conducted under local or regional anaesthesia. During some neurosurgical procedures, the patient is woken up to assess whether surgery has affected, or will affect, important areas.

😐STAGES OF AWARENESS ( Griffith and Jones )

1. Conscious perception with explicit memory;
2. Conscious perception without explicit memory;
3. Dreaming;
4. Subconscious perception with implicit memory;
5. No perception and no implicit memory.

😐CAUSES

🔻may result from a failure of the apparatus to deliver adequate concentrations of anesthetic agent. Such failures include leaks, faulty or empty vaporizers, a misconnected or disconnected breathing system, inaccurate pumps, misplaced venous cannula and occluded infusion tubing

🔻may result from a failure of the clinician  to monitor the concentrations of inspired and expired volatile agents may result in inadequate anesthetic agent being delivered. TIVA is more difficult to monitor in this respect.

🔻may result from an inadequate dosing of the anesthetic agent as represented by the alveolar concentration (it is important to remember that the MAC value that is quoted is only the MAC 50 ) or the computed blood concentration in target-controlled infusion (TCI).

🔻may result from an altered physiology or  pharmacodynamics in the patient e.g. Anxiety may increase dose requirements

🔻may result from the wearing off of the induction agent during a difficult intubation sequence or with the anesthetic techniques for rigid bronchoscopy

😐CLINICAL SIGNS

🔻In the spontaneously breathing patient who is not paralyzed, awareness may be manifest by purposeful movement.

🔻Sympathetic stimulation: the main clinical signs are tachycardia, hypertension, diaphoresis and lacrimation; but their absence does not exclude awareness.  Attempts have been made to quantify these objectively by using the PRST scoring system (blood Pressure, heart Rate, Sweating, Tear formation)..

😐SEQUELAE:

Commonest is the occurrence of a post-traumatic stress syndrome, whose typical features may include nightmares, insomnia, panic attacks and agoraphobia.

😐CHECKLIST FOLLOWING A COMPLAINT OF AWARENESS DURING GENERAL ANAESTHESIA

1. Visit the patient as soon as possible, along with a witness (Preferably a consultant)
2. Take a full history and document the patient’s exact memory of events
3. Attempt to confirm the validity of the account
4. Keep your own copy of the account
5. Give a full explanation to the patient
6. Offer the patient follow-up, including psychological support, and document that this has been offered
7. Reassure the patient that they can safely have further general anaesthetics, with minimal risk of a further episode of awareness
8. If the cause is not known, try to determine it
9. Notify your medical defence organisation
10. Notify your hospital administration
11. Notify the patient’s GP

#awareness , #ptsd , #AnesthesiaComplications , #TheLayMedicalMan , From www.facebook.com/drunnikrishnanz , partial reference from frca.uk , #anaesthesia

Tapentadol

🚩Is a new centrally acting analgesic that relies on a dual mechanism of action. These are mu opioid receptor agonism and norepinephrine (noradrenaline) reuptake inhibition

🚩It  is  therefore  not  a  classical  opioid,  but represents  a  unique  class  of  analgesic  drug  (MOR-NRI).

🚩It  is  now  registered  for  use  in  the  treatment  of  moderate to severe chronic pain that proves unresponsive to conventional non-narcotic medications in many countries.

🚩Tapentadol  has a  much  lower  affinity  (20  times  less) to  the mu  receptor than morphine,  but its analgesic effect is only around three times less than morphine.

🚩This discrepancy is explained by its inhibitory effect on norepinephrine reuptake, strengthening descending inhibitory pathways of pain control

🚩Tapentadol is  seen  by some  as  similar  to tramadol,  but differs in a number of important points:

▶️It is not a racemic mixture of two enantiomers with different pharmacological effects

▶️Has  no  active  metabolites  (which  are  relevant  for tramadol’s mu opioid receptor agonism)

▶️Has only minimal serotonin effects

🚩This means that interactions with other serotonergic drugs (such as anti-depressants) are unlikely, reliance  on  metabolism  by  the  cytochrome  P450 system  for  increased  efficacy  is  not  required  and  retention of  active  metabolites  causing  potential  adverse  effects  is  not a concern.

NB

🔻Tramadol is a 4 phenyl piperidine analogue of codeine

🔻It has a weak central action at opioid receptors

🔻And also on descending monaminergic pathways (also responsible for the side effects)

🔻Hence known as an atypical centrally acting opioid

🔻It's M1 metabolite has more affinity to opioid receptors than parent compound

🔻So metabolites are important in maintaining efficacy

#Opioids , #Pharmacology , #analgesia , #PalliativeCare , #Pain , #SideEffects , #NewDrugs , #medicine , #anaesthesia

Reference: Recent advances in the pharmacological management of acute and chronic pain Stephan A. Schug, Catherine Goddard, Annals of Palliative Medicine, Vol 3, No 4 October 2014

NEURO #ANATOMY OF THE OLFACTORY SYSTEM : How some smells induce tears and sniffing in you❓

😤 Olfactory receptors1️⃣ are the most important cells of the olfactory epithelium and they are the first order neurons of the cranial nerve I

😤There are approximately 100 million such receptors in the olfactory epithelium found along the roof of the nasal cavity including the superior and upper middle conchae

😤Olfactory receptors project through the cribiform plate in the ethmoid bone

😤They have multiple cilia immersed in a surrounding matrix of mucus and a long dendrite

😤Odiferous chemicals get dissolved in this mucus and then trigger the olfactory receptors

😤The impulses pass through the neuron to the olfactory bulb (lies in base  of frontal  cortex in anterior  fossa), which has projections to cortical areas

😤The primary olfactory area in the temporal lobe process such informations through it's connections with the hypothalamus, thalamus and frontal cortex

😤The other major cell type is basal cells2️⃣ found deep to the olfactory neurons (olfactory neurons have a half-life of one month) and replace them, as they mature

😤3️⃣Sustentacular or supporting cells constitute the columnar mucus epithelium found between the receptors

😤There are 4️⃣Olfactory (Bowman’s) glands found in the connective tissue beneath the olfactory epithelium which produce the mucus in which the odiferous chemicals dissolve

❓➡️ 🅰️ Finally answer to the question

😤The innervation of the olfactory epithelial cells from cranial nerve VII (facial nerve) explains the tears and sniffing evoked by some smells.

Reference: Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology, 8th edn. New York, NY: HarperCollins, 1996; pp. 454–5

#smell , #Olfaction , #PhysiologyForExams , #NeuroAnatomy , #anesthesiology