Alat untuk mengukur kedalaman anestesi

The BIS monitor, licensed by Health Canada, is the first quantitative EEG index used in clinical practice as a
monitor to assess the depth of anesthesia. It consists of a sensor, a digital signal converter, and a monitor. The
sensor is placed on the patient’s forehead to pick up the electrical signals from the cerebral cortex and transfer
them to the digital signal converter. A BIS score quantifies changes in the electrophysiologic state of the brain
during anesthesia. In patients who are awake, a typical BIS score is 90 to 100. Complete suppression of cortical
activity results in a BIS score of 0, known as a flat line. Lower numbers indicate a higher hypnotic effect. Overall,
a BIS value below 60 is associated with a low probability of response to commands. There are several alternative
technologies to quantify the depth of anesthesia, but only the BIS and SNAP monitors are licensed in Canada.

Bispectral index (BIS) is one of several technologies used to monitor depth of anesthesia. BIS monitors are used
to supplement Guedel's classification system for determining depth of anesthesia. Titrating anesthetic agents to
a specific bispectral index during general anesthesia in adults (and children over 1 year old) allows the
anesthetist to adjust the amount of anesthetic agent to the needs of the patient, possibly resulting in a more
rapid emergence from anesthesia. Use of the BIS monitor could reduce the incidence of intraoperative
awareness during anaesthesia.[1] The exact details of the algorithm used to create the BIS index have not been
disclosed by the company that developed it.
BIS cannot be used as the sole monitor of anaesthesia, as it is affected by several other factors, including the
anaesthetic drugs used (BIS is relatively insensitive to agents such as ketamine and nitrous oxide), and muscle
movement or artefact from surgical equipment. BIS is used as an adjunct to monitoring under anaesthesia - its
use has been shown to reduce overall dose of anaesthetic agent used and therefore may improve recovery time
from anaesthesia

Guedel’s classification
Stage I (stage of analgesia or disorientation): from beginning of induction of general anesthesia to loss of
consciousness.
Stage II (stage of excitement or delirium): from loss of consciousness to onset of automatic breathing. Eyelash
reflex disappear but other reflexes remain intact and coughing, vomiting and struggling may occur; respiration
can be irregular with breath-holding.
Stage III (stage of surgical anesthesia): from onset of automatic respiration to respiratory paralysis. It is divided
into four planes:
 Plane I - from onset of automatic respiration to cessation of eyeball movements. Eyelid reflex is lost,
swallowing reflex disappears, marked eyeball movement may occur but conjunctival reflex is lost at the
bottom of the plane
 Plane II - from cessation of eyeball movements to beginning of paralysis of intercostal muscles. Laryngeal
reflex is lost although inflammation of the upper respiratory tract increases reflex irritability, corneal
reflex disappears, secretion of tears increases (a useful sign of light anesthesia), respiration is automatic
and regular, movement and deep breathing as a response to skin stimulation disappears.
 Plane III - from beginning to completion of intercostal muscle paralysis. Diaphragmatic respiration persists
but there is progressive intercostal paralysis, pupils dilated and light reflex is abolished. The laryngeal
reflex lost in plane II can still be initiated by painful stimuli arising from the dilatation of anus or cervix.
This was the desired plane for surgery when muscle relaxants were not used.
 Plane IV - from complete intercostal paralysis to diaphragmatic paralysis (apnea).
Stage IV: from stoppage of respiration till death. Anesthetic overdose-caused medullary paralysis with
respiratory arrest and vasomotor collapse. Pupils are widely dilated and muscles are relaxed.

METHEMOGLOBIN
Methemoglobin terus menerus dibentuk di dalam eritrosit pada jumlah kecil karena disebabkan oksidasi
spontan.[2] Senyawa ini dicegah oleh sistem enzim untuk terakumulasi di eritrosit sehingga jumlah
methemoglobin hanya sebesar kurang dari 1% dari jumlah total hemoglobin. [2] Methemoglobin berwarna coklat
kebiruan dan tidak akan berubah menjadi merah saat terpapar oksigen.[2] Besi yang teroksidasi tidak mampu
mengikat oksigen, namun saat satu atau lebih atom besi telah teroksidasi, maka konformasi molekul hemoglobin
akan berubah.[2] Hal ini menyebabkan afinitas oksigen dari kelompok heme akan meningkat.[2] Jika jumlah
methemoglobin meningkat di darah, maka kurva disosiasi oksigen akan bergeser ke kiri, dan oksigen tidak
tersalurkan dengan efisien ke jaringan tubuh.[2] Jika methemoglobin berjumlah lebih besar dari 30% dari total
hemoglobin, maka akan timbul gejala penyakit hipoksia dan sianosis.[2] Jumlah methemoglobin yang meningkat
adalah hasil produksi yang berlebihan yang disebabkan oleh keberadaan senyawa pengoksidasi (contohnya nitrit)
atau jika adanya pengurangan aktivitas enzim methemoglobin reduktase (yang biasanya terjadi karena kelainan
genetik).[2] Jumlah berlebih ini juga ditemukan pada penderita kelainan turunan penyakit Hb M yang
menyebabkan ketidaknormalan pada struktur bagian globin dari molekul hemoglobin.
MetHb is a form of the oxygen-carrying metalloprotein hemoglobin, in which the iron in the heme group is in the
Fe3+ (ferric) state, not the Fe2+ (ferrous) of normal hemoglobin. Methemoglobin cannot bind oxygen, unlike
oxyhemoglobin.[2] It is bluish chocolate-brown in color. In human blood a trace amount of methemoglobin is
normally produced spontaneously, but when present in excess the blood becomes abnormally dark bluish brown.
The NADH-dependent enzyme methemoglobin reductase (a type of diaphorase) is responsible for converting
methemoglobin back to hemoglobin.
Normally one to two percent of a person's hemoglobin is methemoglobin; a higher percentage than this can be
genetic or caused by exposure to various chemicals and depending on the level can cause health problems
known as methemoglobinemia. A higher level of methemoglobin will tend to cause a pulse oximeter to read
closer to 85% regardless of the true level of oxygen saturation.[3]

Methemoglobin saturation
Methemoglobin saturation is expressed as the percentage of hemoglobin in the methemoglobin state; That is
MetHb as a proportion of Hb.
 1-2% Normal
 Less than 10% metHb - No symptoms
 10-20% metHb - Skin discoloration only (most notably on mucous membranes)
 20-30% metHb - Anxiety, headache, dyspnea on exertion
 30-50% metHb - Fatigue, confusion, dizziness, tachypnea, palpitations
 50-70% metHb - Coma, seizures, arrhythmias, acidosis
 Greater than 70% metHb - Death

WIND UP PHENOMENON
Pain wind-up is the perceived increase in pain intensity over time when a given stimulus is delivered repeatedly
above a critical rate. It is caused by repeated stimulation of group C peripheral nerve fibers, leading to
progressively increasing electrical response in the corresponding spinal cord (posterior horn) neurons due to
priming of the NMDA receptor based response